Psychology and Neuroscience Faculty Database
Psychology and Neuroscience
Arts & Sciences
Duke University

 HOME > Arts & Sciences > pn > Faculty    Search Help Login pdf version printable version 

Publications of Richard S. Surwit    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds305793,
   Author = {Surwit, RS and Ross, SL and Feinglos, MN},
   Title = {Stress, behavior, and glucose control in diabetes
             mellitus},
   Pages = {97-118},
   Publisher = {LAWRENCE ERLBAUM ASSOC PUBL},
   Editor = {MCCABE, PM and SCHNEIDERMAN, N and FIELD, TM and SKYLER,
             JS},
   Year = {2013},
   Month = {May},
   ISBN = {9780805804089},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1991BT22L00005&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Doi = {10.4324/9780203771723},
   Key = {fds305793}
}

@article{fds305767,
   Author = {Lane, JD and Kuhn, CM and Surwit, RS and Siegler, IC and Brummett, BH and Williams, RB},
   Title = {BLOOD PRESSURE 'NON-DIPPING' STATUS IS ASSOCIATED WITH
             GREATER OVERNIGHT EPINEPHRINE EXCRETION},
   Journal = {Psychosomatic Medicine},
   Volume = {75},
   Number = {3},
   Pages = {A31-A31},
   Publisher = {LIPPINCOTT WILLIAMS & WILKINS},
   Year = {2013},
   Month = {April},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000330467400104&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305767}
}

@article{fds305766,
   Author = {Georgiades, A and Brummett, BH and Siegler, IC and Surwit, RS and Kuhn,
             C and Grichnik, K and Stafford-Smith, M and Williams,
             RB},
   Title = {EFFECT OF CENTRAL NERVOUS SYSTEM SEROTONIN FUNCTION ON
             INFLAMMATION, ADIPOSITY AND INSULIN SENSITIVITY},
   Journal = {Psychosomatic Medicine},
   Volume = {75},
   Number = {3},
   Pages = {A69-A69},
   Publisher = {LIPPINCOTT WILLIAMS & WILKINS},
   Year = {2013},
   Month = {April},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000330467400220&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305766}
}

@article{fds305778,
   Author = {Surwit, RS and Williams, RB and Georgiades, A},
   Title = {Adrenal Medullary Function, Adiposity and Fasting
             Glucose},
   Journal = {Obesity (Silver Spring, Md.)},
   Volume = {19},
   Pages = {S92-S92},
   Publisher = {NATURE PUBLISHING GROUP},
   Year = {2011},
   Month = {November},
   ISSN = {1930-7381},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000296603100200&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305778}
}

@article{fds305788,
   Author = {Georgiades, A and Williams, RB and Lane, JD and Boyle, SH and Brummett,
             BH and Siegler, IC and Barefoot, JC and Kuhn, CM and Surwit,
             RS},
   Title = {Plasma Epinephrine Levels Determine Fasting and Stress
             Induced Glucose Levels in Women With High Central
             Adiposity},
   Journal = {Obesity (Silver Spring, Md.)},
   Volume = {17},
   Pages = {S54-S54},
   Publisher = {NATURE PUBLISHING GROUP},
   Year = {2009},
   Month = {November},
   ISSN = {1930-7381},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000271237800023&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305788}
}

@article{fds305795,
   Author = {Surwit, RS and Kuhn, CM and Helms, MJ and Siegler, IC and Feinglos, MN and Williams, RB},
   Title = {MAO-uVNTR is related to CNS serotonergic function, glucose
             metabolism, BMI, and hostility},
   Journal = {Diabetes},
   Volume = {55},
   Pages = {A431-A431},
   Publisher = {AMER DIABETES ASSOC},
   Year = {2006},
   Month = {June},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000238055802498&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305795}
}

@article{fds305792,
   Author = {Kuhn, CM and Gadde, K and Schanberg, SM and Marchuk, DA and Siegler, IC and Surwit, RS and Williams, RB},
   Title = {Serotonin transporter polymorphism influences the prolactin
             response to tryptophan and stress},
   Journal = {Neuropsychopharmacology},
   Volume = {30},
   Pages = {S141-S141},
   Publisher = {NATURE PUBLISHING GROUP},
   Year = {2005},
   Month = {December},
   ISSN = {0893-133X},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000233442100375&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305792}
}

@article{fds305811,
   Author = {Collins, S and Surwit, RS and Wang, SY and Daniel, KW and Petro, AE and Snedden, SK},
   Title = {Regulation of the uncoupling protein genes (UCP-1,-2,-3) by
             nutrients and hormones},
   Journal = {Progress in Obesity Research: 8},
   Pages = {373-379},
   Publisher = {JOHN LIBBEY & CO},
   Editor = {GuyGrand, B},
   Year = {1999},
   Month = {January},
   ISBN = {0-86196-581-7},
   ISSN = {0962-7936},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000084261200044&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305811}
}

@article{fds6169,
   Author = {R.S. Surwit and Williams, P.},
   Title = {Animal models provide insight into psychosomatic factors in
             diabetes},
   Journal = {Psychosomatic Medicine},
   Volume = {58},
   Pages = {582-589},
   Year = {1996},
   Key = {fds6169}
}

@article{fds305799,
   Author = {SURWIT, RS and MCCASKILL, CC and ROSS, SL and FEINGLOS,
             MN},
   Title = {BEHAVIORAL AND PHARMACOLOGICAL MANIPULATION OF
             GLUCOSE-TOLERANCE IN TYPE-II DIABETES},
   Journal = {Diabetes 1991},
   Volume = {1000},
   Pages = {1227-1230},
   Publisher = {ELSEVIER SCIENCE PUBL B V},
   Editor = {RIFKIN, H and COLWELL, JA and TAYLOR, SI},
   Year = {1991},
   Month = {January},
   ISBN = {0-444-89254-0},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1991BV33Y00233&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305799}
}


%% Papers Published   
@article{fds348806,
   Author = {Surwit, RS and Williams, RB and Siegler, IC and Lane, JD and Helms, M and Applegate, KL and Zucker, N and Feinglos, MN and McCaskill, CM and Barefoot, JC},
   Title = {Erratum. Hostility, race, and glucose metabolism in
             nondiabetic individuals. Diabetes Care 2002;25:835-839.},
   Journal = {Diabetes Care},
   Volume = {43},
   Number = {3},
   Pages = {691},
   Year = {2020},
   Month = {March},
   url = {http://dx.doi.org/10.2337/dc20-er03},
   Doi = {10.2337/dc20-er03},
   Key = {fds348806}
}

@article{fds332663,
   Author = {Merwin, RM and Moskovich, AA and Honeycutt, LK and Lane, JD and Feinglos, M and Surwit, RS and Zucker, NL and Dmitrieva, NO and Babyak,
             MA and Batchelder, H and Mooney, J},
   Title = {Time of Day When Type 1 Diabetes Patients With Eating
             Disorder Symptoms Most Commonly Restrict
             Insulin.},
   Journal = {Psychosom Med},
   Volume = {80},
   Number = {2},
   Pages = {222-229},
   Year = {2018},
   url = {http://dx.doi.org/10.1097/PSY.0000000000000550},
   Abstract = {OBJECTIVE: Restricting insulin to lose weight is a
             significant problem in the clinical management of type 1
             diabetes (T1D). Little is known about this behavior or how
             to effectively intervene. Identifying when insulin
             restriction occurs could allow clinicians to target typical
             high-risk times or formulate hypotheses regarding factors
             that influence this behavior. The current study investigated
             the frequency of insulin restriction by time of day.
             METHODS: Fifty-nine adults with T1D and eating disorder
             symptoms completed 72 hours of real-time reporting of eating
             and insulin dosing with continuous glucose monitoring. We
             used a generalized estimating equation model to test the
             global hypothesis that frequency of insulin restriction
             (defined as not taking enough insulin to cover food
             consumed) varied by time of day, and examined frequency of
             insulin restriction by hour. We also examined whether
             patterns of insulin restriction for 72 hours corresponded
             with patients' interview reports of insulin restriction for
             the past 28 days. RESULTS: Frequency of insulin restriction
             varied as a function of time (p = .016). Insulin restriction
             was the least likely in the morning hours (6:00-8:59 AM),
             averaging 6% of the meals/snacks consumed. Insulin
             restriction was more common in the late afternoon (3:00-5:59
             PM), peaking at 29%. Insulin was restricted for 32% of the
             meals/snacks eaten overnight (excluding for hypoglycemia);
             however, overnight eating was rare. Insulin restriction was
             associated with higher 120-minute postprandial blood glucose
             (difference = 44.4 mg/dL, 95% confidence interval =
             22.7-68.5, p < .001) and overall poorer metabolic control (r
             = 0.43-0.62, p's < .01). Patients reported restricting
             insulin for a greater percentage of meals and snacks for the
             past 28 days than during the 72 hour real-time assessment;
             however, the reports were correlated (Spearman's ρ = 0.46,
             p < .001) and accounted for similar variance in HbA1c (34%
             versus 35%, respectively). CONCLUSIONS: Findings suggest
             that insulin restriction may be less likely in the morning,
             and that late afternoon is a potentially important time for
             additional therapeutic support. Results also suggest that
             systematic clinical assessment and treatment of overnight
             eating might improve T1D management.},
   Doi = {10.1097/PSY.0000000000000550},
   Key = {fds332663}
}

@article{fds305765,
   Author = {Merwin, RM and Dmitrieva, NO and Honeycutt, LK and Moskovich, AA and Lane, JD and Zucker, NL and Surwit, RS and Feinglos, M and Kuo,
             J},
   Title = {Momentary Predictors of Insulin Restriction Among Adults
             With Type 1 Diabetes and Eating Disorder
             Symptomatology.},
   Journal = {Diabetes Care},
   Volume = {38},
   Number = {11},
   Pages = {2025-2032},
   Year = {2015},
   Month = {November},
   ISSN = {0149-5992},
   url = {http://dx.doi.org/10.2337/dc15-0753},
   Abstract = {OBJECTIVE: Individuals with type 1 diabetes who restrict
             insulin to control weight are at high risk for
             diabetes-related complications and premature death. However,
             little is known about this behavior or how to effectively
             intervene. The aim of the current study was to identify
             predictors of insulin restriction in the natural environment
             that might inform new treatment directions. RESEARCH DESIGN
             AND METHODS: Eighty-three adults with type 1 diabetes and a
             range of eating disorder symptomatology completed 3 days of
             ecological momentary assessment. Participants reported
             emotions, eating, and insulin dosing throughout the day
             using their cellular telephone. Linear mixed models were
             used to estimate the effects of heightened negative affect
             (e.g., anxiety) before eating and characteristics of the
             eating episode (e.g., eating a large amount of food) on the
             risk of insulin restriction. RESULTS: Individuals who
             reported greater-than-average negative affect (general
             negative affect and negative affect specifically about
             diabetes) during the study period were more likely to
             restrict insulin. Momentary increases in anxiety/nervousness
             and guilt/disgust with self before eating (relative to an
             individual's typical level) further increased the odds of
             restricting insulin at the upcoming meal. Insulin
             restriction was more likely when individuals reported that
             they broke a dietary rule (e.g., "no desserts").
             CONCLUSIONS: Results suggest that insulin restriction might
             be decreased by helping patients with type 1 diabetes
             respond effectively to heightened negative affect (e.g.,
             anxiety, guilt) and encouraging patients to take a less
             rigid, punitive approach to diabetes management.},
   Doi = {10.2337/dc15-0753},
   Key = {fds305765}
}

@article{fds276311,
   Author = {Boyle, SH and Georgiades, A and Brummett, BH and Barefoot, JC and Siegler, IC and Matson, WR and Kuhn, CM and Grichnik, K and Stafford-Smith, M and Williams, RB and Kaddurah-Daouk, R and Surwit,
             RS},
   Title = {Associations between central nervous system serotonin,
             fasting glucose, and hostility in African American
             females.},
   Journal = {Annals of Behavioral Medicine : a Publication of the Society
             of Behavioral Medicine},
   Volume = {49},
   Number = {1},
   Pages = {49-57},
   Year = {2015},
   Month = {February},
   ISSN = {0883-6612},
   url = {http://dx.doi.org/10.1007/s12160-014-9626-7},
   Abstract = {BACKGROUND: Previous research has shown an association
             between hostility and fasting glucose in African American
             women. Central nervous system serotonin activity is
             implicated both in metabolic processes and in hostility
             related traits. PURPOSE: The purpose of this study is to
             determine whether central nervous system serotonin
             influences the association between hostility and fasting
             glucose in African American women. METHODS: The study
             consisted of 119 healthy volunteers (36 African American
             women, 27 White women, 21 White males, and 35 African
             American males, mean age 34 ± 8.5 years). Serotonin
             related compounds were measured in cerebrospinal fluid.
             Hostility was measured by the Cook-Medley Hostility Scale.
             RESULTS: Hostility was associated with fasting glucose and
             central nervous system serotonin related compounds in
             African American women only. Controlling for the serotonin
             related compounds significantly reduced the association of
             hostility to glucose. CONCLUSIONS: The positive correlation
             between hostility and fasting glucose in African American
             women can partly be explained by central nervous system
             serotonin function.},
   Doi = {10.1007/s12160-014-9626-7},
   Key = {fds276311}
}

@article{fds276310,
   Author = {Merwin, RM and Moskovich, AA and Dmitrieva, NO and Pieper, CF and Honeycutt, LK and Zucker, NL and Surwit, RS and Buhi,
             L},
   Title = {Disinhibited eating and weight-related insulin mismanagement
             among individuals with type 1 diabetes.},
   Journal = {Appetite},
   Volume = {81},
   Pages = {123-130},
   Year = {2014},
   Month = {October},
   ISSN = {0195-6663},
   url = {http://dx.doi.org/10.1016/j.appet.2014.05.028},
   Abstract = {OBJECTIVE: Withholding insulin for weight control is a
             dangerous practice among individuals with type 1 diabetes;
             yet little is known about the factors associated with this
             behavior. Studies of nondiabetic individuals with weight
             concerns suggest that eating in a disinhibited manner (e.g.,
             binge eating) predicts the use of maladaptive compensatory
             strategies (e.g., self-induced vomiting). The purpose of
             this study was to test whether individuals with type 1
             diabetes are less restrained in their eating when they think
             their blood glucose (BG) is low and whether this contributes
             to insulin omission for weight control purposes and
             subsequently higher hemoglobin A1c (HbA1c). METHODS:
             Two-hundred and seventy-six individuals with type 1 diabetes
             completed an online survey of eating behaviors, insulin
             dosing and most recent HbA1c. We used structural equation
             modeling to test the hypothesis that disinhibited eating
             when blood sugar is thought to be low predicts
             weight-related insulin mismanagement, and this, in turn,
             predicts higher HbA1c. RESULTS: The majority of participants
             endorsed some degree of disinhibition when they think their
             blood glucose is low (e.g., eating foods they do not
             typically allow) and corresponding negative affect (e.g.,
             guilt/shame). The frequency of disinhibited eating was
             positively associated with weight-related insulin
             mismanagement. Controlling for age, sex, education, and
             insulin pump use, the model explained 31.3% of the variance
             in weight-related insulin mismanagement and 16.8% of the
             variance in HbA1c. CONCLUSION: Addressing antecedents to
             disinhibited eating that are unique to type 1 diabetes
             (e.g., perceived BG level) and associated guilt or shame may
             reduce weight-related insulin omission.},
   Doi = {10.1016/j.appet.2014.05.028},
   Key = {fds276310}
}

@article{fds329825,
   Author = {Feinglos, M and Surwit, R and Mehr, SR},
   Title = {The how and why of stress, diabetes, and the
             brain.},
   Journal = {Am J Manag Care},
   Volume = {20},
   Number = {8 Spec No.},
   Pages = {E3},
   Year = {2014},
   Month = {May},
   Key = {fds329825}
}

@article{fds276312,
   Author = {Feinglos, MN and Gibb, RD and Ramsey, DL and Surwit, RS and McRorie,
             JW},
   Title = {Psyllium improves glycemic control in patients with type-2
             diabetes mellitus},
   Journal = {Bioactive Carbohydrates and Dietary Fibre},
   Volume = {1},
   Number = {2},
   Pages = {156-161},
   Publisher = {Elsevier BV},
   Year = {2013},
   Month = {April},
   ISSN = {2212-6198},
   url = {http://dx.doi.org/10.1016/j.bcdf.2013.02.003},
   Abstract = {Objective: This double-blind, placebo-controlled clinical
             study was designed to evaluate the effects of psyllium on
             fasting blood glucose (FBG) and HbA1c in patients being
             treated for type-2 diabetes mellitus (T2DM). Research design
             and methods: Patients were randomly assigned to 1 of the 3
             treatment groups: placebo, psyllium 3.4 g BID or psyllium
             6.8 g BID (just prior to breakfast and dinner). Patients had
             a total of 9 clinic visits during the 20-week study period
             (8 weeks baseline, 12 weeks treatment). A total of 37
             patients [12 females, 34 Caucasians, mean age 62 years] were
             enrolled (8 in the placebo group, 15 in the psyllium 3.4 g
             BID group and 14 in the psyllium 6.8 g BID group) and were
             included in the Intent-to-Treat analysis. Results: Both
             doses of psyllium significantly (p<0.05) lowered FBG
             compared to placebo at treatment weeks 4, 8, and 12.
             Psyllium 6.8 g BID significantly lowered HbA 1c compared to
             placebo at Week 8 (-0.58±0.18, p=0.003), and both the 3.4 g
             dose and the 6.8 g dose of psyllium significantly (p<0.05)
             lowered HbA1c compared to placebo at Week 12 (-0.53±0.20,
             p=0.013; -0.65±0.20, p=0.003, respectively). Conclusions:
             The improvement in glycemic control observed with psyllium
             in T2DM patients was above that already conferred by a
             restricted diet (all patients) and a stable dose of a
             sulfonylurea (81.1% of patients). These data support that
             psyllium is an effective co-therapy for improving glycemic
             control in patients being treated for T2DM. NCT01582282. ©
             2013 Elsevier Ltd.},
   Doi = {10.1016/j.bcdf.2013.02.003},
   Key = {fds276312}
}

@article{fds305813,
   Author = {Lane, JD and Lane, AJ and Surwit, RS and Kuhn, CM and Feinglos,
             MN},
   Title = {Pilot Study of Caffeine Abstinence for Control of Chronic
             Glucose in Type 2 Diabetes.},
   Journal = {Journal of Caffeine Research},
   Volume = {2},
   Number = {1},
   Pages = {45-47},
   Year = {2012},
   Month = {May},
   ISSN = {2156-5783},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23209999},
   Abstract = {BACKGROUND: A growing body of evidence suggests that
             caffeinated beverages may impair chronic glucose control in
             type 2 diabetes. This pilot study tested the chronic effects
             of caffeine abstinence on glucose control in type 2 diabetic
             patients who were daily coffee drinkers. METHODS: Twelve
             coffee drinkers (six males) with established type 2 diabetes
             participated. Seven (five males) completed 3 months of total
             caffeine abstinence. Measures of chronic glucose control,
             long-term (hemoglobin A1c [HbA1c]) and short-term
             (1,5-anhydroglucitol [1,5-AG]), were collected at baseline
             and during follow-up. Abstinence was established by diaries
             confirmed by saliva caffeine assays. RESULTS: Abstinence
             produced significant decreases in HbA1c and increases in
             1,5-AG, both indicating improvements in chronic glucose
             control. Fasting glucose and insulin did not change, nor
             were changes in body weight observed. CONCLUSIONS: Although
             preliminary, these results suggest that caffeine abstinence
             may be beneficial for patients with type 2 diabetes. This
             hypothesis should be confirmed in larger controlled clinical
             trials.},
   Doi = {10.1089/jcr.2012.0003},
   Key = {fds305813}
}

@article{fds305812,
   Author = {Surwit, RS and Williams, RB and Lane, JD and Boyle, SH and Brummett, BH and Siegler, IC and Barefoot, JC and Kuhn, CM and Gerogiades,
             A},
   Title = {EPINEPHRINE, TRUNK FAT AND FASTING GLUCOSE},
   Journal = {Annals of Behavioral Medicine},
   Volume = {43},
   Pages = {S155-S155},
   Publisher = {SPRINGER},
   Year = {2012},
   Month = {April},
   ISSN = {0883-6612},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000302092400600&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305812}
}

@article{fds276341,
   Author = {Brummett, BH and Babyak, MB and Siegler, IC and Surwit, R and Georgiades, A and Boyle, SH and Williams, RB},
   Title = {Systolic blood pressure and adiposity: examination by race
             and gender in a nationally representative sample of young
             adults.},
   Journal = {Am J Hypertens},
   Volume = {25},
   Number = {2},
   Pages = {140-144},
   Year = {2012},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21976277},
   Abstract = {BACKGROUND: Adiposity, or more specifically, underlying body
             fat distribution, has been associated with systolic blood
             pressure (SBP), and it has been suggested that these
             associations vary between whites and blacks, as well as by
             gender. METHODS: Here, we use data from the National
             Longitudinal Study of Adolescent Health (Add Health), a US
             study of over 15,000 participants (median age 29.0 years),
             to characterize the associations between measures of body
             fat distribution-waist circumference (WC) and WC adjusted
             for body mass index (BMI) (WC(-bmi))-with SBP within white
             and black race and gender subgroups. RESULTS: Our findings
             suggest that, at lower levels of WC(-bmi), white women have
             significantly higher SBP as compared to black women, whereas
             black men have higher SBP than white men. Black women with
             WC(-bmi) >90 cm have higher SBP compared to white women with
             similar WC(-bmi), whereas among black and white men the
             associations are essentially similar across the full range
             of WC(-bmi). CONCLUSIONS: The present results suggest that
             associations among anthropometric measures of adiposity and
             blood pressure are nonlinear, and importantly, vary for
             whites and blacks by gender. In black women, SBP increased
             more as WC increased from low- to mid-range levels, whereas
             it was only at higher WC levels that black men exhibited
             higher SBP than white men.},
   Doi = {10.1038/ajh.2011.177},
   Key = {fds276341}
}

@article{fds276334,
   Author = {Surwit, RS and Williams, RB and Lane, JD and Feinglos, MN and Kuhn, CM and Georgiades, A},
   Title = {Plasma epinephrine predicts fasting glucose in centrally
             obese African-American women.},
   Journal = {Obesity (Silver Spring)},
   Volume = {18},
   Number = {9},
   Pages = {1683-1687},
   Year = {2010},
   Month = {September},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20300086},
   Abstract = {The high prevalence of diabetes in African-American (AA)
             women has been widely assumed to be related to the greater
             prevalence of obesity in this group. Catecholamine release
             acting on central adipose tissue has been proposed to be a
             contributing factor. The aim of this article was to examine
             the interaction of plasma catecholamines and central
             adiposity on fasting and nonfasting glucose levels in two
             separate samples. In both studies, the women were healthy,
             nondiabetic of similar age. In addition, both studies
             assessed plasma epinephrine (EPI) and norepinephrine
             (NOREPI) levels collected at three time points. In study 1,
             catecholamines were measured during a standardized
             laboratory mental stress task and in study 2, they were
             measured during the initial phase (10 min) of an intravenous
             glucose tolerance test (IVGTT). Results from both studies
             revealed significant effects of EPI on fasting glucose in
             the obese women. In study 1, mean EPI levels were
             significantly related to fasting glucose in AA women with
             high trunk fat (beta = 0.60, P < 0.001). Because high BMI
             was associated with high trunk fat in women, we used BMI >30
             as a proxy for high trunk fat (>32%) in study 2. In study 2,
             EPI response to the glucose bolus was a strong predictor of
             fasting glucose in AA women with BMI >30 (beta = 0.75, P <
             0.003). We conclude that the effect of central adiposity on
             fasting glucose may be moderated by plasma EPI. This
             suggests that adrenal medullary activity could play a role
             in the pathophysiology of type 2 diabetes.},
   Doi = {10.1038/oby.2010.43},
   Key = {fds276334}
}

@article{fds276345,
   Author = {Williams, RB and Surwit, RS and Siegler, IC and Ashley-Koch, AE and Collins, AL and Helms, MJ and Georgiades, A and Boyle, SH and Brummett,
             BH and Barefoot, JC and Grichnik, K and Stafford-Smith, M and Suarez,
             EC and Kuhn, CM},
   Title = {Central nervous system serotonin and clustering of
             hostility, psychosocial, metabolic, and cardiovascular
             endophenotypes in men.},
   Journal = {Psychosom Med},
   Volume = {72},
   Number = {7},
   Pages = {601-607},
   Year = {2010},
   Month = {September},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20595415},
   Abstract = {OBJECTIVE: To use measures of cerebrospinal fluid (CSF)
             5-hydroxyindoleacetic acid (5HIAA) and genotype of a
             functional polymorphism of the monoamine oxidase A gene
             promoter (MAOA-uVNTR) to study the role of central nervous
             system (CNS) serotonin in clustering of hostility, other
             psychosocial, metabolic and cardiovascular endophenotypes.
             METHODS: In 86 healthy male volunteers, we evaluated CSF
             levels of the primary serotonin metabolite 5HIAA and
             MAOA-uVNTR genotype for association with a panel of 29
             variables assessing hostility, other psychosocial,
             metabolic, and cardiovascular endophenotypes. RESULTS: The
             correlations of 5HIAA with these endophenotypes in men with
             more active MAOA-uVNTR alleles were significantly different
             from those of men with less active alleles for 15 of the 29
             endophenotypes. MAOA-uVNTR genotype and CSF 5HIAA interacted
             to explain 20% and 22% of the variance, respectively, in
             scores on one factor wherein high scores reflected a less
             healthy psychosocial profile and a second factor wherein
             high score reflected increased insulin resistance, body mass
             index, blood pressure and hostility. In men with less active
             alleles, higher 5HIAA was associated with more favorable
             profiles of hostility, other psychosocial, metabolic and
             cardiovascular endophenotypes; in men with more active
             alleles, higher 5HIAA was associated with less favorable
             profiles. CONCLUSIONS: These findings indicate that, in men,
             indices of CNS serotonin function influence the expression
             and clustering of hostility, other psychosocial, metabolic
             and cardiovascular endophenotypes that have been shown to
             increase risk of developing cardiovascular disease. The
             findings are consistent with the hypothesis that increased
             CNS serotonin is associated with a more favorable
             psychosocial/metabolic/cardiovascular profile, whereas
             decreased CNS serotonin function is associated with a less
             favorable profile.},
   Doi = {10.1097/PSY.0b013e3181eb9d67},
   Key = {fds276345}
}

@article{fds276333,
   Author = {Surwit, RS and Lane, JD and Millington, DS and Zhang, H and Feinglos,
             MN and Minda, S and Merwin, R and Kuhn, CM and Boston, RC and Georgiades,
             A},
   Title = {Hostility and minimal model of glucose kinetics in African
             American women.},
   Journal = {Psychosom Med},
   Volume = {71},
   Number = {6},
   Pages = {646-651},
   Year = {2009},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19561162},
   Abstract = {OBJECTIVE: To explore the underlying physiology of hostility
             (HOST) and to test the hypothesis that HOST has a greater
             impact on fasting glucose in African American (AA) women
             than it does on AA men or white men or women, using an
             intravenous glucose tolerance test (IVGTT) and the minimal
             model of glucose kinetics. METHODS: A total of 115 healthy
             subjects selected for high or low scores on the 27 item Cook
             Medley HOST Scale underwent an IVGTT. Fasting nonesterified
             fatty acids (NEFA) levels were measured before the IVGTT.
             Catecholamine levels were measured 10 minutes into the
             IVGTT. RESULTS: Moderation by group (AA women versus others)
             of HOST was found for glucose effectiveness (Sg, p = .02),
             acute insulin response (AIRg, p = .02), and disposition
             index (DI, p = .02). AA women showed a negative association
             between HOST and both Sg (beta = -0.45, p = .04) and DI
             (beta = -0.49, p = .02), controlling for age and body mass
             index. HOST was also associated with changes in epinephrine
             (beta = 0.39, p = .05) and fasting NEFA (beta = 0.44, p =
             .02) in the AA women. Controlling for fasting NEFA reduced
             the effect of HOST on both Sg and DI. CONCLUSIONS: This
             study shows that HOST is related to decreased DI, a measure
             of pancreatic compensation for increased insulin resistance
             as well as decreased Sg, a measure of noninsulin-mediated
             glucose transport compared in AA women. These effects are
             partly mediated by the relationship of HOST to fasting
             NEFA.},
   Doi = {10.1097/PSY.0b013e3181acee4c},
   Key = {fds276333}
}

@article{fds276338,
   Author = {Georgiades, A and Lane, JD and Boyle, SH and Brummett, BH and Barefoot,
             JC and Kuhn, CM and Feinglos, MN and Williams, RB and Merwin, R and Minda,
             S and Siegler, IC and Suarez, EC and Surwit, RS},
   Title = {Hostility and fasting glucose in African American
             women.},
   Journal = {Psychosom Med},
   Volume = {71},
   Number = {6},
   Pages = {642-645},
   Year = {2009},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19553288},
   Abstract = {OBJECTIVE: To examine whether the relationship of hostility
             (HOST) to fasting glucose indices is moderated by sex and
             race. HOST has been associated with abnormalities in glucose
             metabolism. Prior studies suggested that this association
             may be more prevalent in women and in African American (AA)
             individuals. METHODS: A total of 565 healthy AA and white
             (W) men and women (mean age = 33 +/- 6 years) were assessed.
             HOST was measured by the 27-item version of the Cook Medley
             HOST Scale. The moderating effects of sex and race were
             evaluated for the associations of HOST to fasting glucose,
             insulin, and insulin sensitivity (HOMA-IR). RESULTS:
             Analysis showed a moderating effect of sex and race on the
             association of HOST to fasting glucose (p = .03), but not
             for insulin (p = .12). Analysis of HOMA-IR revealed a trend
             (p = .06) for the interaction. Stratified analyses by race
             and sex revealed a positive association between HOST and
             fasting glucose only in AA women, which remained significant
             after controlling for age and body mass index. CONCLUSION: A
             relationship between HOST and fasting glucose was evident in
             AA women only, a group that has twice the risk of developing
             Type 2 diabetes compared with W women. Further studies are
             needed to elucidate the mechanisms by which HOST may affect
             glucose metabolism in AA women.},
   Doi = {10.1097/PSY.0b013e3181acee3a},
   Key = {fds276338}
}

@article{fds276340,
   Author = {Newgard, CB and An, J and Bain, JR and Muehlbauer, MJ and Stevens, RD and Lien, LF and Haqq, AM and Shah, SH and Arlotto, M and Slentz, CA and Rochon, J and Gallup, D and Ilkayeva, O and Wenner, BR and Yancy, WS and Eisenson, H and Musante, G and Surwit, R and Millington, DS and Butler,
             MD and Svetkey, LP},
   Title = {A Branched-Chain Amino Acid-Related Metabolic Signature that
             Differentiates Obese and Lean Humans and Contributes to
             Insulin Resistance (DOI:10.1016/j.cmet.2009.02.002)},
   Journal = {Cell Metabolism},
   Volume = {9},
   Number = {6},
   Pages = {565-566},
   Publisher = {Elsevier BV},
   Year = {2009},
   Month = {May},
   ISSN = {1550-4131},
   url = {http://dx.doi.org/10.1016/j.cmet.2009.05.001},
   Doi = {10.1016/j.cmet.2009.05.001},
   Key = {fds276340}
}

@article{fds276339,
   Author = {Newgard, CB and An, J and Bain, JR and Muehlbauer, MJ and Stevens, RD and Lien, LF and Haqq, AM and Shah, SH and Arlotto, M and Slentz, CA and Rochon, J and Gallup, D and Ilkayeva, O and Wenner, BR and Yancy, WS and Eisenson, H and Musante, G and Surwit, RS and Millington, DS and Butler,
             MD and Svetkey, LP},
   Title = {A branched-chain amino acid-related metabolic signature that
             differentiates obese and lean humans and contributes to
             insulin resistance.},
   Journal = {Cell Metab},
   Volume = {9},
   Number = {4},
   Pages = {311-326},
   Year = {2009},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19356713},
   Abstract = {Metabolomic profiling of obese versus lean humans reveals a
             branched-chain amino acid (BCAA)-related metabolite
             signature that is suggestive of increased catabolism of BCAA
             and correlated with insulin resistance. To test its impact
             on metabolic homeostasis, we fed rats on high-fat (HF), HF
             with supplemented BCAA (HF/BCAA), or standard chow (SC)
             diets. Despite having reduced food intake and a low rate of
             weight gain equivalent to the SC group, HF/BCAA rats were as
             insulin resistant as HF rats. Pair-feeding of HF diet to
             match the HF/BCAA animals or BCAA addition to SC diet did
             not cause insulin resistance. Insulin resistance induced by
             HF/BCAA feeding was accompanied by chronic phosphorylation
             of mTOR, JNK, and IRS1Ser307 and by accumulation of multiple
             acylcarnitines in muscle, and it was reversed by the mTOR
             inhibitor, rapamycin. Our findings show that in the context
             of a dietary pattern that includes high fat consumption,
             BCAA contributes to development of obesity-associated
             insulin resistance.},
   Doi = {10.1016/j.cmet.2009.02.002},
   Key = {fds276339}
}

@article{fds276325,
   Author = {Zhang, H and Stevens, RD and Young, SP and Surwit, R and Georgiades, A and Boston, R and Millington, DS},
   Title = {A convenient LC-MS method for assessment of glucose kinetics
             in vivo with D-[13C6]glucose as a tracer.},
   Journal = {Clin Chem},
   Volume = {55},
   Number = {3},
   Pages = {527-532},
   Year = {2009},
   Month = {March},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19181735},
   Abstract = {BACKGROUND: The isotope-labeled intravenous glucose
             tolerance test (IVGTT) combined with computer modeling is
             widely used to derive parameters related to glucose
             metabolism in vivo. Most of these methods involve use of
             either (2)H(2)-labeled or (13)C(1)-labeled D-glucose as a
             tracer with GC-MS to measure the isotope enrichment. These
             methods are challenging, both technologically and
             economically. We have developed a novel approach that is
             suitable for labeled-IVGTT studies involving a large cohort
             of individuals. METHODS: The tracer, D-[(13)C(6)]glucose, is
             a low-cost alternative with the significant advantage that
             the sixth isotope of natural glucose has virtually zero
             natural abundance, which facilitates isotopomer analysis
             with <1% labeled glucose in the infusate. After
             deproteinization of plasma samples collected at various
             times, glucose is converted to a stable derivative, purified
             by solid-phase extraction (SPE), and analyzed by
             HPLC-electrospray ionization mass spectrometry to accumulate
             the isotope-abundance data for the A+2, A+3, and A+6 ions of
             the glucose derivative. A 2-pool modeling program was used
             to derive standard kinetic parameters. RESULTS: With
             labeled-IVGTT data from 10 healthy male individuals, the
             values for insulin sensitivity, glucose effectiveness, and
             the plasma clearance rate estimated with the 2-pool minimal
             model compared well with values obtained via traditional
             methods. CONCLUSIONS: The relative simplicity and robustness
             of the new method permit the preparation and analysis of up
             to 48 samples/day, a throughput equivalent to 2 complete
             IVGTT experiments, and this method is readily adaptable to
             existing 96 well-format purification and analytical
             systems.},
   Doi = {10.1373/clinchem.2008.113654},
   Key = {fds276325}
}

@article{fds276344,
   Author = {Brummett, BH and Boyle, SH and Siegler, IC and Kuhn, CM and Surwit, RS and Garrett, ME and Collins, A and Ashley-Koch, A and Williams,
             RB},
   Title = {HPA axis function in male caregivers: effect of the
             monoamine oxidase-A gene promoter (MAOA-uVNTR).},
   Journal = {Biol Psychol},
   Volume = {79},
   Number = {2},
   Pages = {250-255},
   Year = {2008},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18639608},
   Abstract = {Caregiving stress is associated with negative health
             outcomes. Neuroendocrine functioning may be a mediator of
             such outcomes. The MAOA gene regulates activity of
             neurotransmitters involved with neuroendocrine responses to
             stress. Differences in polymorphisms of this gene have been
             shown to influence susceptibility to stress. Therefore, we
             examined allelic variation in MAOA-uVNTR, a functional
             polymorphism of MAOA, as a moderator of chronic stress
             effects on urinary cortisol excretion in 74 males enrolled
             in a case/control study of caregivers for relatives with
             dementia. Mixed models analysis of variance were used to
             examine MAOA-uVNTR genotype (3 repeats vs. 3.5/4 repeats) as
             a moderator of the impact of stress (caregiver vs.
             non-caregiver) on the urinary excretion pattern (overnight,
             daytime, evening) of cortisol. Caregivers with MAOA-uVNTR
             alleles associated with less transcriptional activity
             (3-repeats) displayed a pattern of cortisol excretion -- a
             decrease from overnight to daytime -- that was suggestive of
             HPA axis blunting, as compared to non-caregivers and those
             caregivers with the more active alleles (3.5/4 repeats)
             (cortisol p<.043). Individuals with less active MAOA-uVNTR
             alleles who are under chronic stress may be at increased
             risk for exhaustion of the HPA response to such
             stress.},
   Doi = {10.1016/j.biopsycho.2008.06.004},
   Key = {fds276344}
}

@article{fds276346,
   Author = {O'Shea, SI and Arcasoy, MO and Samsa, G and Cummings, SE and Thames, EH and Surwit, RS and Ortel, TL},
   Title = {Direct-to-patient expert system and home INR monitoring
             improves control of oral anticoagulation.},
   Journal = {Journal of Thrombosis and Thrombolysis},
   Volume = {26},
   Number = {1},
   Pages = {14-21},
   Year = {2008},
   Month = {August},
   ISSN = {0929-5305},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17616845},
   Abstract = {BACKGROUND AND OBJECTIVE: Internet-based disease management
             programs have the potential to improve patient care. The
             objective of this study was to determine whether an
             interactive, internet-based system enabling supervised,
             patient self-management of oral anticoagulant therapy
             provided management comparable to an established
             anticoagulation clinic. PATIENTS/METHODS: Sixty patients
             receiving chronic oral anticoagulant therapy who had access
             to the internet and a printer, were enrolled into this
             prospective, single-group, before-after study from a single
             clinic and managed between March 2002 and January 2003.
             Patients learned how to use a home prothrombin time monitor
             and how to access the system through the internet. Patients
             used the system for six months, with daily review by the
             supervising physician. The primary outcome variable was the
             difference in time in therapeutic range prior to and
             following introduction of internet-supervised patient
             self-management. RESULTS: The mean time in therapeutic range
             increased from 63% in the anticoagulation clinic (control
             period) to 74.4% during internet-supervised patient
             self-management (study period). The mean difference score
             between control and study periods was 11.4% (P = 0.004, 95%
             confidence interval 5.5-17.3%). There were no hemorrhagic or
             thromboembolic complications. CONCLUSIONS: This novel
             approach of internet-supervised patient self-management
             improved time in therapeutic range compared to an
             anticoagulation clinic. This is the first demonstration of
             an internet-based expert system enabling remote and
             effective management of patients on oral anticoagulants.
             Expert systems may be applicable for management of other
             chronic diseases.},
   Doi = {10.1007/s11239-007-0068-y},
   Key = {fds276346}
}

@article{fds276332,
   Author = {Lane, JD and Feinglos, MN and Surwit, RS},
   Title = {Caffeine increases ambulatory glucose and postprandial
             responses in coffee drinkers with type 2
             diabetes.},
   Journal = {Diabetes Care},
   Volume = {31},
   Number = {2},
   Pages = {221-222},
   Year = {2008},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17977936},
   Doi = {10.2337/dc07-1112},
   Key = {fds276332}
}

@article{fds276343,
   Author = {Williams, RB and Marchuk, DA and Siegler, IC and Barefoot, JC and Helms,
             MJ and Brummett, BH and Surwit, RS and Lane, JD and Kuhn, CM and Gadde, KM and Ashley-Koch, A and Svenson, IK and Suarez, EC and Schanberg,
             SM},
   Title = {Childhood socioeconomic status and serotonin transporter
             gene polymorphism enhance cardiovascular reactivity to
             mental stress.},
   Journal = {Psychosom Med},
   Volume = {70},
   Number = {1},
   Pages = {32-39},
   Year = {2008},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18158371},
   Abstract = {OBJECTIVE: To test the hypothesis that low socioeconomic
             status (SES) and the 5HTTLPR L allele are associated with
             increased cardiovascular reactivity (CVR) to stress in a
             larger sample and that SES and 5HTTLPR genotypes interact to
             enhance CVR to stress. CVR to mental stress has been
             proposed as one mechanism linking stress to the pathogenesis
             of cardiovascular disease. The more transcriptionally
             efficient long (L) allele of a polymorphism of the serotonin
             transporter gene promoter (5HTTLPR) has been found
             associated with increased risk of myocardial infarction. We
             found the long allele associated with larger CVR to mental
             stress in a preliminary study of 54 normal volunteers.
             METHODS: Subjects included 165 normal community volunteers
             stratified for race, gender, and SES, who underwent mental
             stress testing. RESULTS: Childhood SES as indexed by
             Father's Education Level was associated with larger systolic
             blood pressure (SBP) (p < .05) and diastolic blood pressure
             (DBP) (p = .01) responses to mental stress. The L allele was
             associated with larger SBP (p = .04), DBP (p < .0001), and
             heart rate (p = .04) responses to mental stress compared
             with the short (S) allele. Subjects with the SS genotype and
             high Father's Education exhibited smaller SBP (5.2 mm Hg)
             and DBP (2.9 mm Hg) responses than subjects with LL genotype
             and low Father's Education (SBP = 13.3 mm Hg, p = .002; DBP
             = 9.7 mm Hg, p < .0001). CONCLUSIONS: Both the 5HTTLPR long
             allele and low SES, particularly during childhood, are
             associated with increased CVR to mental stress, which could
             account, at least in part, for the increased cardiovascular
             disease risk associated with these characteristics. If
             confirmed in further research, these characteristics could
             be used to identify persons who might benefit from
             preventive interventions.},
   Doi = {10.1097/PSY.0b013e31815f66c3},
   Key = {fds276343}
}

@article{fds305808,
   Author = {Lane, JD and Prince, C and Feinglos, MN and Surwit,
             RS},
   Title = {CAFFEINE EXAGGERATES POSTPRANDIAL INSULIN RESISTANCE IN
             ADULTS AT RISK FOR TYPE 2 DIABETES},
   Journal = {Annals of Behavioral Medicine},
   Volume = {33},
   Pages = {S33-S33},
   Publisher = {SPRINGER},
   Year = {2007},
   Month = {December},
   ISSN = {0883-6612},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000261185300124&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305808}
}

@article{fds276337,
   Author = {Boyle, SH and Surwit, RS and Georgiades, A and Brummett, BH and Helms,
             MJ and Williams, RB and Barefoot, JC},
   Title = {Depressive symptoms, race, and glucose concentrations: the
             role of cortisol as mediator.},
   Journal = {Diabetes Care},
   Volume = {30},
   Number = {10},
   Pages = {2484-2488},
   Year = {2007},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17630268},
   Abstract = {OBJECTIVE: This study examined the associations of
             depressive symptoms with glucose concentrations and morning
             cortisol levels in 665 African-American and 4,216 Caucasian
             Vietnam-era veterans. RESEARCH DESIGN AND METHODS: Glucose
             level was measured as a three-level variable (diabetes,
             impaired glucose, and normal). Depressive symptoms were
             measured by the Obvious Depression Scale (OBD) from the
             Minnesota Multiphasic Personality Inventory. RESULTS:
             Regression models showed significant race x OBD interactions
             in relation to glucose concentration (P < 0.0001) and
             cortisol (P < 0.0001). The OBD was positively associated
             with glucose concentration and cortisol in both racial
             groups. However, the magnitude of those associations was
             larger for African Americans. Further analyses suggested
             that cortisol partially mediated the race difference in the
             relation of depressive symptoms to glucose concentrations.
             CONCLUSIONS: These results suggest that enhanced
             hypothalamic pituitary adrenal activity plays an important
             role in the relation of depressive symptoms to dysregulated
             glucose metabolism and may partially explain the
             differential effects of depressive symptoms on glucose
             levels in African-American and Caucasian male
             subjects.},
   Doi = {10.2337/dc07-0258},
   Key = {fds276337}
}

@article{fds276342,
   Author = {Brummett, BH and Krystal, AD and Siegler, IC and Kuhn, C and Surwit, RS and Züchner, S and Ashley-Koch, A and Barefoot, JC and Williams,
             RB},
   Title = {Associations of a regulatory polymorphism of monoamine
             oxidase-A gene promoter (MAOA-uVNTR) with symptoms of
             depression and sleep quality.},
   Journal = {Psychosom Med},
   Volume = {69},
   Number = {5},
   Pages = {396-401},
   Year = {2007},
   Month = {June},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17585061},
   Abstract = {OBJECTIVE: To examine the relationships among the variable
             number of tandem repeats in the monoamine oxidase-A linked
             polymorphic region allelic variation (MAOA-uVNTR) and the
             symptoms of depression and sleep quality. The monoamine
             oxidase-A (MAOA) gene, which plays a vital role in
             degradation of neurotransmitters such as serotonin,
             norepinephrine, and dopamine, contains a polymorphism in its
             promoter region (MAOA-uVNTR) that affects transcriptional
             efficiency. MAOA-uVNTR genotype has been associated with
             both psychological and physical measures. METHODS: The
             sample consisted of 74 males enrolled in a case/control
             study of caregivers for relatives with dementia. Age- and
             race-adjusted linear regression models were used to examine
             the association between low versus high MAOA-uVNTR activity
             alleles, symptoms of depression (Center for Epidemiological
             Studies of Depression), and sleep quality ratings
             (Pittsburgh Sleep Quality Index). RESULTS: MAOA-uVNTR
             alleles associated with less transcriptional activity were
             related to increased symptoms of depression (p < .04;
             Cohen's d = 0.52) and poorer sleep quality (p < .04; Cohen's
             d = 0.31). CONCLUSIONS: Individuals with less active
             MAOA-uVNTR alleles may be at increased risk for depressive
             symptoms and poor sleep.},
   Doi = {10.1097/PSY.0b013e31806d040b},
   Key = {fds276342}
}

@article{fds276347,
   Author = {Georgiades, A and Zucker, N and Friedman, KE and Mosunic, CJ and Applegate, K and Lane, JD and Feinglos, MN and Surwit,
             RS},
   Title = {Changes in depressive symptoms and glycemic control in
             diabetes mellitus.},
   Journal = {Psychosom Med},
   Volume = {69},
   Number = {3},
   Pages = {235-241},
   Year = {2007},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17420441},
   Abstract = {OBJECTIVE: To investigate if changes in depressive symptoms
             would be associated with changes in glycemic control over a
             12-month period in patients with Type 1 and Type 2 diabetes.
             METHODS: Ninety (Type 1 diabetes, n = 28; Type 2 diabetes, n
             = 62) patients having Beck Depression Inventory (BDI) levels
             of >10 were enrolled in the study. Of those 90 patients, 65
             patients completed a 12-week cognitive behavioral therapy
             intervention. BDI was assessed at baseline and thereafter
             biweekly during 12 months. Hemoglobin (HbA1c) and fasting
             blood glucose levels were assessed at baseline and at four
             quarterly in-hospital follow-up visits. Linear mixed-model
             analysis was applied to determine the effects of time and
             diabetes type on depressive symptoms, HbA1c levels, and
             fasting glucose levels. RESULTS: Mean and standard deviation
             baseline BDI and HbA1c levels were 17.9 +/- 5.8 and 7.6 +/-
             1.6, respectively, with no significant difference between
             patients with Type 1 and Type 2 diabetes. Mixed-model
             regression analysis found no difference between the groups
             with Type 1 and Type 2 diabetes in the within-subject effect
             of BDI score on HbA1c or fasting glucose levels during the
             study. Depressive symptoms decreased significantly (p =
             .0001) and similarly over a 12-month period in both patients
             with Type 1 and Type 2 diabetes, whereas HbA1c and fasting
             glucose levels did not change significantly over time in
             either group. CONCLUSION: Changes in depressive symptoms
             were not associated with changes in HbA1c or fasting glucose
             levels over a 1-year period in either patients with Type 1
             or Type 2 diabetes.},
   Doi = {10.1097/PSY.0b013e318042588d},
   Key = {fds276347}
}

@article{fds276331,
   Author = {Lane, JD and Hwang, AL and Feinglos, MN and Surwit,
             RS},
   Title = {Exaggeration of postprandial hyperglycemia in patients with
             type 2 diabetes by administration of caffeine in
             coffee.},
   Journal = {Endocr Pract},
   Volume = {13},
   Number = {3},
   Pages = {239-243},
   Year = {2007},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17599854},
   Abstract = {OBJECTIVE: To test whether caffeine administered in coffee
             increases postprandial hyperglycemia in patients with type 2
             diabetes who are habitual coffee drinkers. METHODS: The
             study used a within-subject, double-blind,
             placebo-controlled experimental design. Twenty adult coffee
             drinkers (11 women and 9 men) with type 2 diabetes treated
             with diet, exercise, orally administered antidiabetic
             agents, or some combination of these factors completed two
             mixed-meal tolerance tests (MMTT) after an overnight fast.
             Before the MMTT, each study participant received 250 mg of
             caffeine in 16 oz (475 mL) of decaffeinated coffee or
             decaffeinated coffee alone, with the treatment order
             counterbalanced in the group. Fasting and 1-hour and 2-hour
             postprandial blood samples were collected for measurement of
             plasma glucose and insulin concentrations. RESULTS: Glucose
             and insulin responses to the MMTT were quantified by the
             incremental areas under the 2-hour concentration-time curves
             (AUC2h). Administration of caffeine in decaffeinated coffee
             increased postprandial glucose and insulin responses (both P
             = 0.02). The mean plasma glucose AUC2h was 28% larger and
             the mean plasma insulin AUC2h was 19% larger after
             administration of caffeine than after administration of
             placebo. CONCLUSION: Other constituents in coffee did not
             prevent the exaggeration of postprandial hyperglycemia by
             caffeine in these patients with type 2 diabetes, who were
             habitual coffee drinkers. Repeated on a daily basis, such
             effects could impair long-term glucose control in those
             patients with type 2 diabetes who habitually drink coffee or
             other caffeinated beverages.},
   Doi = {10.4158/EP.13.3.239},
   Key = {fds276331}
}

@article{fds276330,
   Author = {Surwit, RS and van Tilburg, MAL and Parekh, PI and Lane, JD and Feinglos, MN},
   Title = {Treatment regimen determines the relationship between
             depression and glycemic control.},
   Journal = {Diabetes Research and Clinical Practice},
   Volume = {69},
   Number = {1},
   Pages = {78-80},
   Year = {2005},
   Month = {July},
   ISSN = {0168-8227},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15955389},
   Abstract = {UNLABELLED: Several recent studies have suggested that
             depression is related to poorer glycemic control in patients
             with type 1 diabetes, but not in type 2 diabetes. We
             hypothesize that complexity of self-care regimen rather than
             the type of diabetes, is more important in determining this
             relationship of depression to glycemic control. METHODS: One
             thousand thirty-four adults with diabetes were recruited for
             the study. These patients were treated with: diet and
             exercise, oral medications, oral medications and insulin,
             1-2 daily injections of insulin, and > or =3 daily
             injections. All participants completed the Beck depression
             inventory (BDI) and had a hemoglobin A(1c) (HbA(1c))
             performed as part of routine clinical care. RESULTS: Pearson
             correlations between BDI scores and HbA(1c) were low and
             insignificant in all groups (0.015< or =r< or =0.066) except
             for those administering three or more daily shots of insulin
             (r=0.284; p=0.034). DISCUSSION: The results of this study
             clearly show that while depressive symptoms are
             significantly correlated to glycemic control in patients
             taking three or more insulin injections per day, there is no
             relationship in patients who are taking fewer than three
             injections per day.},
   Doi = {10.1016/j.diabres.2004.11.002},
   Key = {fds276330}
}

@article{fds276336,
   Author = {Brummett, BH and Siegler, IC and Rohe, WM and Barefoot, JC and Vitaliano, PP and Surwit, RS and Feinglos, MN and Williams,
             RB},
   Title = {Neighborhood characteristics moderate effects of caregiving
             on glucose functioning.},
   Journal = {Psychosom Med},
   Volume = {67},
   Number = {5},
   Pages = {752-758},
   Year = {2005},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16204434},
   Abstract = {OBJECTIVE: Adverse neighborhood environments and caregiving
             for a relative with dementia are both stressors that have
             been associated with poor health. The present study examined
             the extent to which three self-report measures of
             neighborhood characteristics interact with caregiving status
             (caregiver versus noncaregiver) to modify an important
             stress related health outcome: plasma glucose. METHODS: The
             study sample consisted of 147 community recruited caregivers
             and 147 participants who did not have caregiving
             responsibilities. We hypothesized that negative neighborhood
             characteristics would magnify effects of caregiving on
             plasma glucose levels. Regression analyses were conducted to
             examine the interaction of three neighborhood characteristic
             measures with caregiving status in predicting fasting plasma
             glucose (FPG) and glycosylated hemoglobin concentration
             (HbA1c), with control for age, race, gender, relation to
             care recipient (spouse or relative), body mass index,
             income, and education. RESULTS: Of the three neighborhood
             measures, the one reflecting crime concerns significantly
             moderated the effect of caregiving on FPG (p < .002) and
             HbA1c (p < .001). For participants with better neighborhood
             characteristics, caregivers and noncaregivers were similar
             with respect to indicators of glucose metabolism; however,
             for participants with worse neighborhood characteristics,
             caregivers had higher levels of FPG and HbA1c, as compared
             with noncaregivers. CONCLUSIONS: Poor health outcomes, such
             as impaired glucose control, may be found among caregivers
             who fear neighborhood crime.},
   Doi = {10.1097/01.psy.0000174171.24930.11},
   Key = {fds276336}
}

@article{fds276329,
   Author = {Lane, JD and Barkauskas, CE and Surwit, RS and Feinglos,
             MN},
   Title = {Caffeine impairs glucose metabolism in type 2
             diabetes.},
   Journal = {Diabetes Care},
   Volume = {27},
   Number = {8},
   Pages = {2047-2048},
   Year = {2004},
   Month = {August},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15277438},
   Doi = {10.2337/diacare.27.8.2047},
   Key = {fds276329}
}

@article{fds276322,
   Author = {Petro, AE and Cotter, J and Cooper, DA and Peters, JC and Surwit, SJ and Surwit, RS},
   Title = {Fat, carbohydrate, and calories in the development of
             diabetes and obesity in the C57BL/6J mouse.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {53},
   Number = {4},
   Pages = {454-457},
   Year = {2004},
   Month = {April},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15045691},
   Abstract = {We have previously shown that the C57BL/6J (B6) mouse will
             develop obesity and diabetes if raised on a high-fat diet.
             Because high fat feeding is associated with hyperphagia, the
             present study was designed to separate the effects of fat
             from those of excess caloric consumption in this animal
             model. B6 mice were fed a low-fat diet (LF group) diet,
             high-fat diet (HF group) diet, or high-fat-restricted diet
             (HFR group), in which intake animals were pair-fed a
             high-fat diet to caloric level consumed by LF for 11 weeks.
             Within 3 weeks, HFR were significantly heavier than LF and,
             after 11 weeks, weight and glucose levels, but not insulin,
             were significantly increased in HFR when compared to LF.
             Body composition analysis showed the weight increase in HFR
             arose from an increase in percent fat consumed. We conclude
             that reducing the number of kilocalories consumed from a
             high-fat diet attenuates but does not prevent the
             development of type 2 diabetes and obesity in the B6
             mouse.},
   Doi = {10.1016/j.metabol.2003.11.018},
   Key = {fds276322}
}

@article{fds276323,
   Author = {Collins, S and Martin, TL and Surwit, RS and Robidoux,
             J},
   Title = {Genetic vulnerability to diet-induced obesity in the
             C57BL/6J mouse: physiological and molecular
             characteristics.},
   Journal = {Physiology & Behavior},
   Volume = {81},
   Number = {2},
   Pages = {243-248},
   Year = {2004},
   Month = {April},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15159170},
   Abstract = {The development of the metabolic syndrome in an increasing
             percentage of the populations of Western societies,
             particularly in the United States, requires valid models for
             establishing basic biochemical changes and performing
             preclinical studies on potential drug targets. The C57BL/6J
             mouse has become an important model for understanding the
             interplay between genetic background and environmental
             challenges such as high-fat/high-calorie diets that
             predispose to the development of the metabolic syndrome.
             This review highlights metabolic and signal transduction
             features that are altered during the course of disease
             progression, many of which mirror the human
             situation.},
   Doi = {10.1016/j.physbeh.2004.02.006},
   Key = {fds276323}
}

@article{fds276383,
   Author = {Berger, JP and Petro, AE and Macnaul, KL and Kelly, LJ and Zhang, BB and Richards, K and Elbrecht, A and Johnson, BA and Zhou, G and Doebber, TW and Biswas, C and Parikh, M and Sharma, N and Tanen, MR and Thompson, GM and Ventre, J and Adams, AD and Mosley, R and Surwit, RS and Moller,
             DE},
   Title = {Distinct properties and advantages of a novel peroxisome
             proliferator-activated protein [gamma] selective
             modulator.},
   Journal = {Molecular Endocrinology (Baltimore, Md.)},
   Volume = {17},
   Number = {4},
   Pages = {662-676},
   Year = {2003},
   Month = {April},
   ISSN = {0888-8809},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12554792},
   Keywords = {Adipocytes • Adipose Tissue • Animals •
             Cardiomegaly • Cells, Cultured • Gene Expression
             Regulation • Hyperglycemia • Indoles •
             Insulin Resistance • Magnetic Resonance Spectroscopy
             • Male • Mice • Mice, Inbred C57BL •
             Models, Molecular • Protein Conformation •
             Receptors, Cytoplasmic and Nuclear • Sulfides •
             Transcription Factors • Weight Gain • agonists*
             • chemically induced • chemistry* • drug
             effects • drug therapy • pharmacology* •
             physiology},
   Abstract = {Antidiabetic thiazolidinediones (TZDs) and non-TZD compounds
             have been shown to serve as agonists of the peroxisome
             proliferator-activated receptor gamma (PPARgamma). Here, we
             report the identification and characterization of a novel
             non-TZD selective PPARgamma modulator (nTZDpa). nTZDpa bound
             potently to PPARgamma with high selectivity vs. PPARalpha or
             PPARdelta. In cell-based assays for transcriptional
             activation, nTZDpa served as a selective, potent PPARgamma
             partial agonist and was able to antagonize the activity of
             PPARgamma full agonists. nTZDpa also displayed partial
             agonist effects when its ability to promote adipogenesis in
             3T3-L1 cells was evaluated. Assessment of protein
             conformation using protease protection or solution nuclear
             magnetic resonance spectroscopy methods showed that nTZDpa
             produced altered PPARgamma conformational stability vs. full
             agonists, thereby establishing a physical basis for its
             observed partial agonism. DNA microarray analysis of RNA
             from 3T3-L1 adipocytes treated with nTZDpa or several
             structurally diverse PPARgamma full agonists demonstrated
             qualitative differences in the affected gene expression
             profile for nTZDpa. Chronic treatment of fat-fed, C57BL/6J
             mice with nTZDpa or a TZD full agonist ameliorated
             hyperglycemia and hyperinsulinemia. However, unlike the TZD,
             nTZDpa caused reductions in weight gain and adipose depot
             size. Feed efficiency was also substantially diminished.
             Unlike TZDs, nTZDpa did not cause cardiac hypertrophy in
             mice. When a panel of PPARgamma target genes was examined in
             white adipose tissue, nTZDpa produced a different in vivo
             expression pattern vs. the full agonist. These findings
             establish that novel selective PPARgamma modulators can
             produce altered receptor conformational stability leading to
             distinctive gene expression profiles, reduced adipogenic
             cellular effects, and potentially improved in vivo
             biological responses. Such compounds may lead to preferred
             therapies for diabetes, obesity, or metabolic
             syndrome.},
   Doi = {10.1210/me.2002-0217},
   Key = {fds276383}
}

@article{fds276321,
   Author = {Brown, NW and Ward, A and Surwit, R and Tiller, J and Lightman, S and Treasure, JL and Campbell, IC},
   Title = {Evidence for metabolic and endocrine abnormalities in
             subjects recovered from anorexia nervosa.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {52},
   Number = {3},
   Pages = {296-302},
   Year = {2003},
   Month = {March},
   url = {http://dx.doi.org/10.1053/meta.2003.50067},
   Abstract = {Subjects with anorexia nervosa (AN) at low weight display
             metabolic, endocrine, and behavioral abnormalities. Whether
             these various differences are a consequence of the condition
             and persist after recovery is unclear. We tested the
             hypothesis that abnormalities in the insulin and leptin axes
             and in the desire to eat persisted in subjects who had
             recovered from AN in terms of body mass index (BMI) and
             menstrual function. Endocrine, metabolic, and psychological
             parameters were assessed by sampling under fasting
             conditions and serially in response to a standard meal.
             Subjects included 18 females recovered from AN and 18 female
             controls and measures included plasma insulin, leptin,
             glucose and beta-hydroxybutyrate (beta-HBA) concentrations
             together with desire to eat. Fasting glucose concentrations
             were normal in both groups, but fasting insulin
             concentrations were significantly lower and the fasting
             glucose/insulin ratio significantly higher in the recovered
             subjects. The glucose concentration was significantly higher
             at the end of the meal period in the recovered group. The
             peak increase of insulin during the meal was significantly
             less in the recovered group and in response to the meal,
             glucose/insulin ratios were significantly higher for the
             first 45 minutes indicating a delayed insulin response.
             Fasting beta-HBA concentrations were not significantly
             different between groups, but postmeal decreases were
             significant and larger in the recovered AN group. Fasting
             and meal-related leptin concentrations were not
             significantly different between the groups and in both
             groups were correlated with BMI. In controls, but not in
             recovered subjects, the reported desire to eat was
             correlated with plasma glucose and leptin concentrations.
             The insulin, glucose and beta-HBA data indicated the
             presence of insulin hypersensitivity in the recovered
             subjects. As the insulin response to the meal was blunted
             and apparently delayed, there may be a persistent alteration
             in pancreatic function as a long-term pathological
             consequence of the anorexia. Alternatively, these data
             indicate a possible trait marker for AN.},
   Doi = {10.1053/meta.2003.50067},
   Key = {fds276321}
}

@article{fds276373,
   Author = {Surwit, RS and Williams, RB and Siegler, IC and Lane, JD and Helms, M and Applegate, KL and Zucker, N and Feinglos, MN and McCaskill, CM and Barefoot, JC},
   Title = {Hostility, race, and glucose metabolism in nondiabetic
             individuals.},
   Journal = {Diabetes Care},
   Volume = {25},
   Number = {5},
   Pages = {835-839},
   Year = {2002},
   Month = {May},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11978677},
   Keywords = {Adult • African Americans • African Continental
             Ancestry Group* • Blood Glucose • Body Mass Index
             • Diabetes Mellitus • European Continental
             Ancestry Group* • Female • Health Behavior* •
             Hostility* • Humans • Insulin • Male •
             Personality • Risk Factors • United States •
             analysis • blood* • epidemiology • ethnology*
             • metabolism* • psychology},
   Abstract = {OBJECTIVE: The present study was designed to determine
             whether hostility is differentially related to measures of
             glucose metabolism in African-Americans and Caucasians.
             RESEARCH DESIGN AND METHODS: The relationship of hostility,
             as measured by a subset of the Cook-Medley hostility scale
             (CMHOST) inventory items, to various parameters of glucose
             metabolism were examined in a young, healthy sample of male
             and female African-American and Caucasian volunteers.
             Fasting blood samples were collected during an inpatient
             admission, at which time the CMHOST was also administered.
             RESULTS: In the entire sample, the CMHOST was found to be
             significantly correlated with fasting glucose and insulin
             sensitivity, as measured by the homeostatic model assessment
             (HOMA). However, the relationship of hostility to these
             parameters of glucose metabolism was different in
             African-American and Caucasian subjects. Hostility was
             significantly related to fasting glucose in
             African-Americans and to insulin sensitivity and fasting
             insulin in Caucasian subjects. The relationship of hostility
             to insulin sensitivity and fasting insulin was partially
             dependent on BMI in Caucasians, but the relationship of
             hostility to fasting glucose was unrelated to BMI in
             African-Americans. CONCLUSIONS: Our data suggest that the
             relationship of hostility to measures of glucose metabolism
             is mediated differently in these two ethnic groups.
             Therefore, hostility seems to be part of a constellation of
             risk-related behaviors related to BMI in Caucasians but
             independently related to fasting glucose in
             African-Americans.},
   Doi = {10.2337/diacare.25.5.835},
   Key = {fds276373}
}

@article{fds276328,
   Author = {Williams, PG and Colder, CR and Lane, JD and McCaskill, CC and Feinglos,
             MN and Surwit, RS},
   Title = {Examination of the neuroticism-symptom reporting
             relationship in individuals with type 2 diabetes},
   Journal = {Personality & Social Psychology Bulletin},
   Volume = {28},
   Number = {8},
   Pages = {1015-1025},
   Publisher = {SAGE Publications},
   Year = {2002},
   Month = {January},
   ISSN = {0146-1672},
   url = {http://dx.doi.org/10.1177/01461672022811001},
   Abstract = {The current study utilized a within-subject, experience
             sampling methodology (ESM) to examine the relationship
             between neuroticism (N) and physical symptom reports.
             Individuals with type 2 diabetes monitored diabetes-related
             symptoms, rated negative and positive affect (NA and PA),
             estimated their blood glucose (BG) levels, and tested their
             actual BG levels with a glucometer four times per day for 7
             days. Multilevel modeling analyses indicated that N, NA, and
             PA were related to reported symptom frequency. Neuroticism
             moderated the relation between PA and symptom reports: Lower
             PA was more strongly related to symptom reports among high-N
             individuals. In addition, there was evidence that symptoms
             mediated the relationship between N and state NA. Finally, N
             was related to overestimation of BG, beyond that accounted
             for by state NA. Results are discussed with respect to
             potential effects of N on the processing of negative
             self-relevant information and on self-regulatory behavior in
             health contexts. © 2002 by the Society for Personality and
             Social Psychology, Inc.},
   Doi = {10.1177/01461672022811001},
   Key = {fds276328}
}

@article{fds276403,
   Author = {Surwit, RS and van Tilburg, MAL and Zucker, N and McCaskill, CC and Parekh, P and Feinglos, MN and Edwards, CL and Williams, P and Lane,
             JD},
   Title = {Stress management improves long-term glycemic control in
             type 2 diabetes.},
   Journal = {Diabetes Care},
   Volume = {25},
   Number = {1},
   Pages = {30-34},
   Year = {2002},
   Month = {January},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11772897},
   Keywords = {Blood Glucose • Continental Population Groups •
             Diabetes Mellitus, Type 2 • Energy Intake • Female
             • Hemoglobin A, Glycosylated • Humans • Male
             • Manifest Anxiety Scale • Middle Aged •
             Patient Compliance • Patient Education •
             Personality Inventory • Questionnaires • Stress,
             Psychological • analysis • blood •
             metabolism* • methods* • prevention & control*
             • psychology* • rehabilitation},
   Abstract = {OBJECTIVE: There is conflicting evidence regarding the
             utility of stress management training in the treatment of
             diabetes. The few studies that have shown a therapeutic
             effect of stress management have used time-intensive
             individual therapy. Unfortunately, widespread use of such
             interventions is not practical. The aim of the present
             investigation is to determine whether a cost-effective,
             group-based stress management training program can improve
             glucose metabolism in patients with type 2 diabetes and to
             determine whether a particular subset of patients is more
             likely to get positive results. RESEARCH DESIGN AND METHODS:
             Patients with type 2 diabetes were randomized to undergo a
             five-session group diabetes education program with or
             without stress management training. Participants (n = 108)
             were followed for 1 year, during which HbA(1c) tests and
             questionnaires assessing perceived stress, anxiety, and
             psychological health were administered at regular intervals
             to evaluate treatment effects. RESULTS: Stress management
             training was associated with a small (0.5%) but significant
             reduction in HbA(1c). Compliance with the treatment regimen
             decreased over time but was similar to that seen in patients
             receiving stress management for other reasons in the clinic.
             Trait anxiety (a measure of stable individual differences in
             anxiety proneness) did not predict response to treatment,
             showing that highly anxious patients did not derive more
             benefit from training. CONCLUSIONS: The current results
             indicate that a cost-effective, group stress management
             program in a "real-world" setting can result in clinically
             significant benefits for patients with type 2
             diabetes.},
   Doi = {10.2337/diacare.25.1.30},
   Key = {fds276403}
}

@article{fds276319,
   Author = {Collins, S and Cao, W and Daniel, KW and Dixon, TM and Medvedev, AV and Onuma, H and Surwit, R},
   Title = {Adrenoceptors, uncoupling proteins, and energy
             expenditure.},
   Journal = {Experimental Biology and Medicine},
   Volume = {226},
   Number = {11},
   Pages = {982-990},
   Year = {2001},
   Month = {December},
   ISSN = {1535-3702},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11743133},
   Abstract = {Interest in the biology of adipose tissue has undergone a
             revival in recent years with the discovery of a host of
             genes that contribute to the regulation of satiety and
             metabolic rate. The catecholamines have long been known to
             be key modulators of adipose tissue lipolysis and the
             hydrolysis of triglyceride energy stores. However, more
             recent efforts to understand the role of individual
             adrenergic receptor subtypes expressed in adipocytes and
             their signal transduction pathways have revealed a
             complexity not previously appreciated. Combined with this
             interest in the modulation of adipocyte metabolism is a
             renewed focus upon brown adipose tissue and the mechanisms
             of whole body thermogenesis in general. The discovery of
             novel homologs of the brown fat uncoupling protein (UCP)
             such as UCP2 and UCP3 has provoked intensive study of these
             mitochondrial proteins and the role that they play in fuel
             metabolism. The story of the novel UCPs has proven to be
             intriguing and still incompletely understood. Here, we
             review the status of adipose tissue from inert storage depot
             to endocrine organ, interesting signal transduction pathways
             triggered by beta-adrenergic receptors in adipocytes, the
             potential of these receptors for discriminating and
             coordinated metabolic regulation, and current views on the
             role of UCP2 and UCP3 based on physiological studies and
             gene knockout models.},
   Doi = {10.1177/153537020122601104},
   Key = {fds276319}
}

@article{fds305779,
   Author = {Petro, AE and Cotter, J and Surwit, SJ and Cooper, DA and Peters, JC and Surwit, RS},
   Title = {Independent effects of fat vs calories on diabetes and
             obesity.},
   Journal = {Obesity Research},
   Volume = {9},
   Pages = {111S-111S},
   Publisher = {NORTH AMER ASSOC STUDY OBESITY},
   Year = {2001},
   Month = {September},
   ISSN = {1071-7323},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000171076300235&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305779}
}

@article{fds305768,
   Author = {Tanen, M and Petro, A and Wu, MS and Doebber, TW and Moller, DE and Surwit,
             RS and Berger, J},
   Title = {Amelioration of diabetes and remodeling of adipose tissue by
             PPAR gamma agonists: Possible roles for uncoupling
             proteins},
   Journal = {Diabetes},
   Volume = {50},
   Pages = {A522-A523},
   Publisher = {AMER DIABETES ASSOC},
   Year = {2001},
   Month = {June},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000168964302154&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305768}
}

@article{fds305804,
   Author = {Wang, YF and Chen, JS and Wang, K and Feinglos, MN and Surwit,
             RS},
   Title = {Diabetes increases the risk of hypertension in young,
             non-obese, urban and rural Chinese},
   Journal = {Diabetes},
   Volume = {50},
   Pages = {A216-A216},
   Publisher = {AMER DIABETES ASSOC},
   Year = {2001},
   Month = {June},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000168964300886&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305804}
}

@article{fds305806,
   Author = {Surwit, RS and Siegler, IC and Feinglos, MN and Helms, MJ and Applegate,
             K and Williams, RB and Scroll, M and Barefoot, JC},
   Title = {Hostility predicts fasting glucose, insulin, and risk for
             type 2 diabetes},
   Journal = {Diabetes},
   Volume = {50},
   Pages = {A85-A85},
   Publisher = {AMER DIABETES ASSOC},
   Year = {2001},
   Month = {June},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000168964300342&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305806}
}

@article{fds276381,
   Author = {Surwit, RS and Collins, S},
   Title = {Revisiting lessons from the C57BL/6J mouse.},
   Journal = {American Journal of Physiology. Endocrinology and
             Metabolism},
   Volume = {280},
   Number = {5},
   Pages = {E825-E826},
   Year = {2001},
   Month = {May},
   ISSN = {0193-1849},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11315708},
   Keywords = {Animals • Leptin • Mice • Mice, Inbred C57BL
             • Mice, Inbred Strains • Obesity • metabolism
             • metabolism* • physiology*},
   Doi = {10.1152/ajpendo.2001.280.5.E825},
   Key = {fds276381}
}

@article{fds276367,
   Author = {Wing, RR and Goldstein, MG and Acton, KJ and Birch, LL and Jakicic, JM and Sallis, JF and Smith-West, D and Jeffery, RW and Surwit,
             RS},
   Title = {Behavioral science research in diabetes: lifestyle changes
             related to obesity, eating behavior, and physical
             activity.},
   Journal = {Diabetes Care},
   Volume = {24},
   Number = {1},
   Pages = {117-123},
   Year = {2001},
   Month = {January},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11194216},
   Keywords = {Behavior Therapy • Behavioral Medicine* • Body
             Weight • Diabetes Mellitus • Diabetes Mellitus,
             Type 2 • Diet • Eating • Exercise •
             Humans • Hyperphagia • Life Style • Obesity
             • Research* • prevention & control •
             prevention & control* • therapy •
             therapy*},
   Abstract = {Lifestyle factors related to obesity, eating behavior, and
             physical activity play a major role in the prevention and
             treatment of type 2 diabetes. In recent years, there has
             been progress in the development of behavioral strategies to
             modify these lifestyle behaviors. Further research, however,
             is clearly needed, because the rates of obesity in our
             country are escalating, and changing behavior for the long
             term has proven to be very difficult. This review article,
             which grew out of a National Institute of Diabetes and
             Digestive and Kidney Diseases conference on behavioral
             science research in diabetes, identifies four key topics
             related to obesity and physical activity that should be
             given high priority in future research efforts: 1)
             environmental factors related to obesity, eating, and
             physical activity; 2) adoption and maintenance of healthful
             eating, physical activity, and weight; 3) etiology of eating
             and physical activity; and 4) multiple behavior changes.
             This review article discusses the significance of each of
             these four topics, briefly reviews prior research in each
             area, identifies barriers to progress, and makes specific
             research recommendations.},
   Doi = {10.2337/diacare.24.1.117},
   Key = {fds276367}
}

@article{fds141567,
   Title = {Surwit, R.S. and Collins, S. Revisting lessons from the
             C57BL/6J mouse. American Journal of Physiology-Endocrinology
             and Metabolism, 2001, 280, E825-E826 (letter).},
   Year = {2001},
   Key = {fds141567}
}

@article{fds141618,
   Title = {Wing, R.R., Goldstein, M.G., Acton, K.J., Birch, L.L.,
             Jakicic, J.M., Sallis, J.F., West, D.S., Jeffrey, R.W., and
             Surwit, R.S. Behavioral science research in diabetes:
             Lifestyle changes related to obesity and physical activity.
             Diabetes Care, 2001, 24, 117-123.},
   Year = {2001},
   Key = {fds141618}
}

@article{fds141619,
   Title = {Van Tilburg, M.A.L., McCaskill, C.C., Lane, J.D., Edwards,
             C.L., Bethel, A., Feinglos, M.N., and Surwit, R.S. Depressed
             mood is a factor in glycemic control in type 1, diabetes.
             Psychosomatic Medicine, 2001, 63, 551-555.},
   Year = {2001},
   Key = {fds141619}
}

@article{fds141620,
   Title = {Collins, S., Cao, W., Daniel, K.W., Dixon, T.M., Medvedev,
             A.V., Onuma, H. and Surwit, R. Adrenoceptors, Uncoupling
             Proteins, and Energy Expenditure. Experimental Biology and
             Medicine 2001 226, 982-990.},
   Year = {2001},
   Key = {fds141620}
}

@article{fds276376,
   Author = {Collins, S and Surwit, RS},
   Title = {The beta-adrenergic receptors and the control of adipose
             tissue metabolism and thermogenesis.},
   Journal = {Recent Progress in Hormone Research},
   Volume = {56},
   Pages = {309-328},
   Year = {2001},
   ISSN = {0079-9963},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11237219},
   Keywords = {Adipose Tissue • Animals • Cell Differentiation
             • Cyclic AMP • Cyclic AMP-Dependent Protein
             Kinases • Humans • MAP Kinase Signaling System
             • Mice • Models, Biological • Obesity •
             Receptors, Adrenergic, beta • Receptors, Adrenergic,
             beta-3 • Signal Transduction • Sympathetic Nervous
             System • Temperature • Time Factors •
             metabolism • metabolism* • physiology*},
   Abstract = {The beta-adrenergic receptors (betaARs) are members of the
             large family of G protein-coupled receptors. There are three
             betaAR subtypes (beta1AR, beta2AR beta3AR), each of which is
             coupled to Galphas and the stimulation of intracellular cAMP
             levels. While beta1AR and beta2AR are broadly expressed
             throughout tissues of the body, beta3AR is found
             predominantly in adipocytes. Stimulation of the betaARs
             leads to lipolysis in white adipocytes and nonshivering
             thermogenesis in brown fat. However, in essentially all
             animal models of obesity, the betaAR system is dysfunctional
             and the ability to stimulate lipolysis and thermogenesis is
             impaired. Nevertheless, we and others have shown that
             selective beta3AR agonists are able to prevent or reverse
             obesity and the loss of betaAR expression and to stimulate
             thermogenesis. This chapter will review the current
             understanding of the role of the sympathetic nervous system
             and the adipocyte betaARs in models of obesity; the
             physiologic impact of changes in betaAR expression on body
             composition and thermogenesis; and the regulation and unique
             properties of betaAR subtypes in brown and white adipocytes.
             The latter includes our recent discovery of novel signal
             transduction mechanisms utilized by beta3AR to activate
             simultaneously the protein kinase A and MAP kinase pathways.
             The impact of understanding these pathways and their
             potential role in modulating adaptive thermogenesis is
             discussed.},
   Doi = {10.1210/rp.56.1.309},
   Key = {fds276376}
}

@article{fds276425,
   Author = {Van Tilburg and MA and McCaskill, CC and Lane, JD and Edwards, CL and Bethel, A and Feinglos, MN and Surwit, RS},
   Title = {Depressed mood is a factor in glycemic control in type 1
             diabetes.},
   Journal = {Psychosomatic Medicine},
   Volume = {63},
   Number = {4},
   Pages = {551-555},
   Year = {2001},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11485108},
   Keywords = {Adult • Aged • Blood Glucose • Depression
             • Diabetes Mellitus, Type 1 • Diabetes Mellitus,
             Type 2 • Female • Hemoglobin A, Glycosylated
             • Humans • Male • Middle Aged •
             Personality Inventory • Sick Role* • blood •
             metabolism* • psychology • psychology*},
   Abstract = {OBJECTIVE: The diabetes literature contains conflicting
             evidence on the relationship between depression and glycemic
             control. This may be due, in part, to the fact that past
             studies failed to distinguish between patients with type 1
             and type 2 diabetes. Because these are actually completely
             different diseases that are often treated differently and
             consequently make different demands on patients, the
             relationship between glycemic control and depressed mood in
             type 1 and type 2 diabetes was examined separately. METHODS:
             The relationship between Beck Depression Inventory (BDI)
             scores and HbA1c, as an index of long-term glycemic control,
             was measured in samples of 30 patients with type 1 and 34
             patients with type 2 diabetes. RESULTS: Groups of patients
             with type 1 and type 2 diabetes did not differ in mean BDI
             score or HbA1c level. Correlation analysis revealed a
             significant positive relationship between BDI scores and
             HbA1c in the type 1 group (r = .44, p < .02) but not in the
             type 2 group (r = -0.06, p > .05). This relationship was
             evident throughout the entire range of BDI scores and was
             not restricted to scores indicative of clinical depression.
             Patients with type 1 diabetes who had higher HbA1c and BDI
             scores reported a lower frequency of home blood glucose
             monitoring. CONCLUSIONS: Variations in depressive mood,
             below the level of clinical depression, are associated with
             meaningful differences in glycemic control in type 1 but not
             type 2 diabetes. Preliminary data analysis suggests that
             this effect may be mediated, at least in part, by decreased
             self-care behaviors in patients with more depressed
             mood.},
   Doi = {10.1097/00006842-200107000-00005},
   Key = {fds276425}
}

@article{fds276324,
   Author = {Watkins, LL and Surwit, RS and Sherwood, A},
   Title = {Glycemic control and impaired autonomic function: Is glucose
             the sole culprit? [11]},
   Journal = {Diabetes Care},
   Volume = {23},
   Number = {12},
   Pages = {1863-1864},
   Year = {2000},
   Month = {December},
   ISSN = {0149-5992},
   Key = {fds276324}
}

@article{fds276317,
   Author = {Arsenijevic, D and Onuma, H and Pecqueur, C and Raimbault, S and Manning, BS and Miroux, B and Couplan, E and Alves-Guerra, MC and Goubern, M and Surwit, R and Bouillaud, F and Richard, D and Collins, S and Ricquier, D},
   Title = {Disruption of the uncoupling protein-2 gene in mice reveals
             a role in immunity and reactive oxygen species
             production.},
   Journal = {Nature Genetics},
   Volume = {26},
   Number = {4},
   Pages = {435-439},
   Year = {2000},
   Month = {December},
   ISSN = {1061-4036},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11101840},
   Abstract = {The gene Ucp2 is a member of a family of genes found in
             animals and plants, encoding a protein homologous to the
             brown fat uncoupling protein Ucp1 (refs 1-3). As Ucp2 is
             widely expressed in mammalian tissues, uncouples respiration
             and resides within a region of genetic linkage to obesity, a
             role in energy dissipation has been proposed. We demonstrate
             here, however, that mice lacking Ucp2 following targeted
             gene disruption are not obese and have a normal response to
             cold exposure or high-fat diet. Expression of Ucp2 is robust
             in spleen, lung and isolated macrophages, suggesting a role
             for Ucp2 in immunity or inflammatory responsiveness. We
             investigated the response to infection with Toxoplasma
             gondii in Ucp2-/- mice, and found that they are completely
             resistant to infection, in contrast with the lethality
             observed in wild-type littermates. Parasitic cysts and
             inflammation sites in brain were significantly reduced in
             Ucp2-/- mice (63% decrease, P<0.04). Macrophages from
             Ucp2-/- mice generated more reactive oxygen species than
             wild-type mice (80% increase, P<0.001) in response to T.
             gondii, and had a fivefold greater toxoplasmacidal activity
             in vitro compared with wild-type mice (P<0.001 ), which was
             absent in the presence of a quencher of reactive oxygen
             species (ROS). Our results indicate a role for Ucp2 in the
             limitation of ROS and macrophage-mediated
             immunity.},
   Doi = {10.1038/82565},
   Key = {fds276317}
}

@article{fds276369,
   Author = {Surwit, RS and Dixon, TM and Petro, AE and Daniel, KW and Collins,
             S},
   Title = {Diazoxide restores beta3-adrenergic receptor function in
             diet-induced obesity and diabetes.},
   Journal = {Endocrinology},
   Volume = {141},
   Number = {10},
   Pages = {3630-3637},
   Year = {2000},
   Month = {October},
   ISSN = {0013-7227},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11014217},
   Keywords = {Adipocytes • Adipose Tissue • Animals • Blood
             Glucose • Body Weight • Diabetes Mellitus •
             Diazoxide • Diet • Energy Intake • Glucose
             • Insulin • Leptin • Lipids • Male
             • Mice • Mice, Inbred Strains • Muscle,
             Skeletal • Obesity • Organ Size • Receptors,
             Adrenergic, beta • Syndrome • adverse effects*
             • analysis • blood • drug effects •
             etiology • metabolism • metabolism* •
             pathology • pharmacology* • physiology •
             physiopathology},
   Abstract = {We previously demonstrated that the expression and function
             of the adipocyte-specific beta3-adrenergic receptor
             (beta3AR) are significantly depressed in single gene and
             diet-induced rodent models of obesity. Furthermore, these
             models are relatively unresponsive to the anti-obesity
             effects of beta3AR agonists. Because all of these models are
             hyperinsulinemic, we hypothesized that hyperinsulinemia
             could be responsible for this abnormality in beta3AR
             function. The goal of this study was to determine whether
             lowering insulin with the K-ATP channel agonist, diazoxide
             (Dz) would reverse the depressed expression and function of
             the beta3AR found in a model of diet-induced diabetes and
             obesity in C57BL/6J (B6) mice. B6 male mice were placed on
             either high fat (HF) or low fat experimental diets. After 4
             weeks, HF-fed mice were assigned to a group: HF or HF
             containing disodium (R,R)-5- [2-( [2-(3-chlorophenyl)-2-hydroxyethyl]-amino]propyl-1,3-benzodioxole-2,2-di
             carboxylate (CL; 0.001%, wt/wt), Dz (0.32%, wt/wt), or their
             combination (CLDz). Dz animals exhibited significantly
             reduced plasma insulin levels as well as increased 3pAR
             expression and agonist-stimulated adenylyl cyclase activity
             in adipocytes. CLDz was more effective in reducing percent
             body fat, lowering nonesterified fatty acids, improving
             glucose tolerance, and reducing feed efficiency than either
             treatment alone.},
   Doi = {10.1210/endo.141.10.7726},
   Key = {fds276369}
}

@article{fds305787,
   Author = {Surwit, RS},
   Title = {Hyperinsulinemia leptin resistance, and obesity},
   Journal = {Obesity Research},
   Volume = {8},
   Pages = {6S-6S},
   Publisher = {NORTH AMER ASSOC STUDY OBESITY},
   Year = {2000},
   Month = {October},
   ISSN = {1071-7323},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000089876100022&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305787}
}

@article{fds276378,
   Author = {Lane, JD and McCaskill, CC and Williams, PG and Parekh, PI and Feinglos,
             MN and Surwit, RS},
   Title = {Personality correlates of glycemic control in type 2
             diabetes.},
   Journal = {Diabetes Care},
   Volume = {23},
   Number = {9},
   Pages = {1321-1325},
   Year = {2000},
   Month = {September},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10977026},
   Keywords = {Adult • Affect • Behavior Therapy • Blood
             Glucose • Blood Glucose Self-Monitoring • Cohort
             Studies • Diabetes Mellitus, Type 2 • Female
             • Hemoglobin A, Glycosylated • Humans •
             Longitudinal Studies • Male • Personality
             Inventory • Personality* • Questionnaires •
             Stress, Psychological • analysis • blood* •
             metabolism* • prevention & control •
             psychology*},
   Abstract = {OBJECTIVE: To determine whether traits of normal personality
             are associated with variations in glycemic control in
             patients with type 2 diabetes. RESEARCH DESIGN AND METHODS:
             A longitudinal cohort study was conducted using data from
             105 type 2 diabetic patients in a clinical trial of a stress
             management intervention. Before treatment assignment,
             patients completed the NEO Personality Inventory, Revised,
             which is a questionnaire inventory measuring 5 major domains
             of normal personality and 30 important traits that define
             these domains. Glycemic control was assessed by measures of
             HbA1c and average blood glucose levels based on 7 days of
             self-monitoring at baseline and at 6 and 12 months.
             Relationships between personality traits and measures of
             glycemic control were examined by correlation and linear
             regression models that were adjusted for age, sex, race,
             duration of diabetes, medication status, and experimental
             treatment. RESULTS: Lower average blood glucose values at
             baseline were associated with higher scores for the
             personality domain of neuroticism and several specific
             traits including anxiety, angry hostility depression,
             self-consciousness, and vulnerability but were associated
             with lower scores for the trait of altruism. Results were
             similar for HbA1c but were not as strong. Follow-up results
             were similar but were less consistent. CONCLUSIONS:
             Personality traits may offer new insights into variations in
             glycemic control in patients with type 2 diabetes undergoing
             standard management. The relative tendency to experience
             fewer negative emotions and to focus on the needs of others
             instead of oneself could prove to be a risk factor for poor
             glycemic control.},
   Doi = {10.2337/diacare.23.9.1321},
   Key = {fds276378}
}

@article{fds276393,
   Author = {Surwit, RS and Edwards, CL and Murthy, S and Petro,
             AE},
   Title = {Transient effects of long-term leptin supplementation in the
             prevention of diet-induced obesity in mice.},
   Journal = {Diabetes},
   Volume = {49},
   Number = {7},
   Pages = {1203-1208},
   Year = {2000},
   Month = {July},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10909979},
   Keywords = {Adipose Tissue • Animals • Blood Glucose •
             Body Temperature • Body Weight • Diet,
             Fat-Restricted • Dietary Fats* • Eating •
             Infusions, Parenteral • Insulin • Leptin •
             Male • Mice • Mice, Inbred A • Mice, Inbred
             C57BL • Motor Activity • Obesity • Organ Size
             • Time Factors • administration & dosage •
             anatomy & histology • blood • drug effects •
             drug effects* • etiology • metabolism •
             pathology • pharmacology* • prevention &
             control*},
   Abstract = {Low plasma leptin levels have been shown to be associated
             with the development of obesity in mice as well as in
             humans. The present study was undertaken to determine if
             raising plasma leptin levels of obesity-prone C57BL/6J (B6)
             mice to those seen in obesity-resistant A/J mice would
             prevent the development of diet-induced obesity.
             Four-week-old B6 (n = 40) and A/J (n = 10) male mice were
             weaned onto a low-fat (11% kcal) diet. When the animals
             weighed 20 g, their diets were changed to a high-fat (HF)
             diet (58% kcal), and a continuous infusion of leptin (0.4 mg
             x kg(-1) x day(-1)) or phosphate-buffered saline (control)
             was started using Alzet minipumps. The A/J mice were not
             treated but were included to monitor the efficacy of the
             minipumps in raising plasma leptin in B6 mice. The mice were
             followed for 12 weeks. Chronic treatment with leptin for 4
             weeks raised plasma levels in B6 mice to that of A/J mice.
             Plasma leptin in B6 control mice remained significantly
             lower than A/J mice through week 4. By week 8, leptin levels
             in the B6 control group had risen and were similar to A/J
             mice. Although there were significant weight differences
             between B6 treated and B6 control groups for 2-3 weeks after
             pump implantation, these differences were transient.
             Ultimately, there were no weight differences between the B6
             treated and B6 control groups. There were no differences in
             plasma glucose between B6 treated and control groups. Plasma
             insulin values were also not different between the 2 groups.
             There was no effect of leptin supplementation on locomotor
             activity or food intake in B6 mice. In summary, this study
             demonstrates that leptin supplementation in animals that
             show low plasma leptin levels in response to fat feeding may
             slow but does not prevent the subsequent development of
             diet-induced obesity.},
   Doi = {10.2337/diabetes.49.7.1203},
   Key = {fds276393}
}

@article{fds276410,
   Author = {Watkins, LL and Surwit, RS and Grossman, P and Sherwood,
             A},
   Title = {Is there a glycemic threshold for impaired autonomic
             control?},
   Journal = {Diabetes Care},
   Volume = {23},
   Number = {6},
   Pages = {826-830},
   Year = {2000},
   Month = {June},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10841004},
   Keywords = {Adult • Analysis of Variance • Autonomic Nervous
             System • Baroreflex • Blood Glucose • Blood
             Pressure • Fasting • Female • Heart Rate
             • Humans • Insulin • Male • Reference
             Values • analysis • blood* • metabolism*
             • physiology*},
   Abstract = {OBJECTIVE: Although hyperglycemia has been recognized as a
             predictor of cardiovascular autonomic neuropathy in diabetic
             patients, the glucose threshold at which autonomic control
             begins to become impaired has not been evaluated. This study
             examined whether fasting plasma glucose (FPG) or fasting
             plasma insulin (FPI) is associated with reductions in
             baroreflex sensitivity (BRS) in healthy volunteers. RESEARCH
             DESIGN AND METHODS: FPG and FPI were measured after an
             overnight fast in 162 healthy volunteers (91 men, 71 women)
             who were 25-44 years of age. BRS was measured with power
             spectral analysis. RESULTS: Univariate analyses showed that
             FPG was negatively correlated with BRS (r = -0.25, P < or =
             0.001) with significant reductions observed in volunteers
             with FPG in the upper 2 quintiles (i.e., 93-124 mg/dl).
             However, after adjustment for other predictors of BRS (e.g.,
             age, blood pressure, and BMI), the relationship between FPG
             and BRS was no longer significant. In contrast, FPI was
             negatively correlated with BRS in univariate analyses (r =
             -0.32, P < 0.0001) as well as after covariate adjustment,
             with close to a 50% reduction in BRS observed in the
             volunteers with insulin values in the highest quintile
             (i.e., 16-36 microU/ml). CONCLUSIONS: These findings suggest
             that high normal levels of FPG are associated with reduced
             autonomic control secondary to the effects of aging,
             obesity, and elevated blood pressure on FPG levels and that
             elevations in FPI are associated with substantial reductions
             in autonomic cardiac control independent of other
             covariates.},
   Doi = {10.2337/diacare.23.6.826},
   Key = {fds276410}
}

@article{fds276335,
   Author = {Wiener, JS and Scales, MT and Hampton, J and King, LR and Surwit, R and Edwards, CL},
   Title = {Long-term efficacy of simple behavioral therapy for daytime
             wetting in children},
   Journal = {The Journal of Urology},
   Volume = {164},
   Number = {3 I},
   Pages = {786-790},
   Year = {2000},
   Month = {January},
   url = {http://dx.doi.org/10.1016/s0022-5347(05)67313-2},
   Abstract = {Purpose: Behavioral therapy has proved benefit for children
             with daytime wetting but most studies have used biofeedback
             techniques and provide no long-term assessment of results.
             We previously reported similar results using simple
             behavioral therapy without biofeedback. We report the
             long-term efficacy of behavioral therapy for daytime
             wetting. Materials and Methods: Our program of behavioral
             therapy included timed voiding, modification of fluid
             intake, positive reinforcement techniques and pelvic floor
             (Kegel) exercises to promote pelvic floor strengthening and
             relaxation. Questionnaires to assess therapeutic efficacy
             were mailed to patients who had completed therapy more than
             1 year previously. Results: A total of 48 patients
             responded. Mean ages at the time of the initial clinic visit
             and questionnaire were 8.2 and 12.9 years, respectively.
             Improvement in symptoms was noted in approximately 74% of
             the cases during the first year following therapy. At a mean
             of 4.7 years after treatment 59.4% of the patients had
             improved daytime urinary control, 51.1% improved daytime
             urinary frequency and 45.6% improved daytime urinary
             urgency. The frequency of urinary tract infections decreased
             in 56.4% of the cases. Measures of psychological well-being
             were also noted to be improved in a majority of patients. A
             total of 77.3% of the patients stated that they would
             recommend the program to others. Conclusions: Simple
             behavioral therapy without biofeedback techniques is an
             effective and durable first line therapy for children with
             daytime wetting.},
   Doi = {10.1016/s0022-5347(05)67313-2},
   Key = {fds276335}
}

@article{fds276419,
   Author = {Williams, PG and Surwit, RS and Babyak, MA and McCaskill,
             CC},
   Title = {Personality predictors of mood related to
             dieting.},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {66},
   Number = {6},
   Pages = {994-1004},
   Year = {1998},
   Month = {December},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9874913},
   Keywords = {Adult • Affect* • Depression • Diet, Reducing
             • Extraversion (Psychology)* • Female •
             Humans • Middle Aged • Neurotic Disorders •
             Obesity • Personality • Psychological Tests •
             Regression Analysis • Self Assessment (Psychology)
             • Weight Loss • methods • physiology •
             psychology • psychology* • therapy*},
   Abstract = {The clinical utility of a model of normal emotional
             functioning (vs. psychopathology) and the moderating effects
             of neuroticism (N) and extraversion (E) on mood were
             examined during a 6-week weight-loss trial. Participants
             were 40 obese women who completed measures of negative
             affect (NA) and positive affect (PA) weekly during the diet
             and measures of anxiety and depression (Beck Depression
             Inventory [BDI]) at pre-, mid-, and postdiet. Results
             indicated that (a) average NA and PA were each uniquely
             related to postdiet BDI scores, (b) N was significantly
             related to NA during the diet and postdiet BDI scores, and
             (c) N and E interacted to predict PA during the diet. The
             results suggest that assessment of personality and normal
             mood variation may be useful additions to weight-loss
             intervention and research.},
   Doi = {10.1037//0022-006x.66.6.994},
   Key = {fds276419}
}

@article{fds276415,
   Author = {Black, BL and Croom, J and Eisen, EJ and Petro, AE and Edwards, CL and Surwit, RS},
   Title = {Differential effects of fat and sucrose on body composition
             in A/J and C57BL/6 mice.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {47},
   Number = {11},
   Pages = {1354-1359},
   Year = {1998},
   Month = {November},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9826212},
   Keywords = {Animals • Body Composition* • Dietary Fats •
             Dietary Sucrose • Intestines • Male • Mice
             • Mice, Inbred C57BL • Species Specificity •
             Sucrase • Weight Gain • administration & dosage*
             • alpha-Glucosidases • enzymology •
             metabolism},
   Abstract = {The C57BL/6 (B6) mouse is more sensitive to the effects of a
             high-fat diet than the A/J strain. The B6 mouse develops
             severe obesity, hyperglycemia, and hyperinsulinemia when fed
             this dietary regimen. This study was conducted to determine
             the effects of dietary fat and sucrose concentrations on
             body composition and intestinal sucrase (EC 3.2.1.48) and
             maltase (EC 3.2.1.20) activity in these two mouse strains.
             High-fat diets, regardless of sucrose content, resulted in
             significant weight gain, higher body fat, and lower body
             protein and water content in both strains of mice. The shift
             toward higher body fat and lower protein and water content
             was far greater in the B6 strain. Low-fat, high-sucrose
             diets resulted in lower body weight in both strains, as well
             as significantly greater body protein content in B6 mice.
             Analysis of intestinal sucrase showed that the enzyme was
             less active in B6 mice when the diet was high in sucrose.
             Both sucrase and maltase had lower activity in the presence
             of high dietary fat in both mouse strains. The percent
             reduction of intestinal enzyme activity due to dietary fat
             was similar in both strains. The B6 mouse exhibits
             disproportionate weight gain and altered body composition on
             a high-fat diet. This coupled with the reduced body weight
             and increased body protein on a low-fat, high-sucrose diet
             suggests that factors-relative to fat metabolism rather than
             sucrose metabolism are responsible for obesity.},
   Doi = {10.1016/s0026-0495(98)90304-3},
   Key = {fds276415}
}

@article{fds141633,
   Author = {PI Parekh and AE Petro and JM Tiller and MN Feinglos and RS
             Surwit},
   Title = {Reversal of diet-induced obesity and diabetes in C57BL/6J
             mice.},
   Journal = {Metabolism: clinical and experimental, UNITED
             STATES},
   Volume = {47},
   Number = {9},
   Pages = {1089-96},
   Year = {1998},
   Month = {September},
   ISSN = {0026-0495},
   Keywords = {Adipose Tissue • Animals • Blood Glucose •
             Body Weight • Diabetes Mellitus, Experimental •
             Dietary Fats • Insulin • Male • Mice •
             Mice, Inbred C57BL • Obesity • Species Specificity
             • administration & dosage* • analysis •
             anatomy & histology • blood • diet
             therapy*},
   Abstract = {We have previously shown that C57BL/6J (B6) mice develop
             severe obesity and diabetes if weaned onto high-fat diets,
             whereas A/J mice tend to be obesity and diabetes-resistant.
             The purpose of this study was to determine if obesity and
             diabetes in the B6 mouse could be completely reversed by
             reducing dietary fat content. After 4 months, both strains
             consumed more calories on a high-fat diet than on a low-fat
             diet, and both strains showed a higher feed efficiency
             (FE=weight gained/calories consumed) on the high-fat diet
             versus the low-fat diet. However, relative to A/J mice, B6
             mice demonstrated a significantly higher FE on the high-fat
             diet. Hyperglycemia, hyperinsulinemia, and increased
             adiposity were apparent in B6 mice after 4 months on the
             high-fat diet regardless of whether the diet was begun at
             weaning or 4 months later. Correlational analyses showed
             that adiposity was strongly related to both insulin and
             glucose levels in B6 mice, but only moderately related to
             insulin levels in A/J mice. In obese B6 mice that were
             switched to a low-fat diet, obesity and diabetes were
             completely reversed. Adiposity, fasting glucose, and fasting
             insulin values in these mice were equivalent to those in B6
             mice of the same age that had spent 8 months on the low-fat
             diet. In summary, our data show that in the B6 mouse the
             severity of diabetes is a direct function of obesity and
             diabetes is completely reversible by reducing dietary
             fat.},
   Key = {fds141633}
}

@article{fds276435,
   Author = {R.S. Surwit and Parekh, PI and Petro, AE and Tiller, JM and Feinglos, MN and Surwit,
             RS},
   Title = {Reversal of diet-induced obesity and diabetes in C57BL/6J
             mice.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {47},
   Number = {9},
   Pages = {1089-1096},
   Year = {1998},
   Month = {September},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9751238},
   Abstract = {We have previously shown that C57BL/6J (B6) mice develop
             severe obesity and diabetes if weaned onto high-fat diets,
             whereas A/J mice tend to be obesity and diabetes-resistant.
             The purpose of this study was to determine if obesity and
             diabetes in the B6 mouse could be completely reversed by
             reducing dietary fat content. After 4 months, both strains
             consumed more calories on a high-fat diet than on a low-fat
             diet, and both strains showed a higher feed efficiency
             (FE=weight gained/calories consumed) on the high-fat diet
             versus the low-fat diet. However, relative to A/J mice, B6
             mice demonstrated a significantly higher FE on the high-fat
             diet. Hyperglycemia, hyperinsulinemia, and increased
             adiposity were apparent in B6 mice after 4 months on the
             high-fat diet regardless of whether the diet was begun at
             weaning or 4 months later. Correlational analyses showed
             that adiposity was strongly related to both insulin and
             glucose levels in B6 mice, but only moderately related to
             insulin levels in A/J mice. In obese B6 mice that were
             switched to a low-fat diet, obesity and diabetes were
             completely reversed. Adiposity, fasting glucose, and fasting
             insulin values in these mice were equivalent to those in B6
             mice of the same age that had spent 8 months on the low-fat
             diet. In summary, our data show that in the B6 mouse the
             severity of diabetes is a direct function of obesity and
             diabetes is completely reversible by reducing dietary
             fat.},
   Doi = {10.1016/s0026-0495(98)90283-9},
   Key = {fds276435}
}

@article{fds141670,
   Author = {JC Barefoot and BL Heitmann and MJ Helms and RB Williams and RS Surwit and IC Siegler},
   Title = {Symptoms of depression and changes in body weight from
             adolescence to mid-life.},
   Journal = {International journal of obesity and related metabolic
             disorders : journal of the International Association for the
             Study of Obesity, ENGLAND},
   Volume = {22},
   Number = {7},
   Pages = {688-94},
   Year = {1998},
   Month = {July},
   ISSN = {0307-0565},
   Keywords = {Adolescent • Adult • Aging • Body Mass Index
             • Depression • Exercise • Female •
             Humans • Longitudinal Studies • Male • Sex
             Characteristics • Smoking • Weight Gain* •
             complications* • physiology • psychology*},
   Abstract = {OBJECTIVE: To investigate the relationship of symptoms of
             depression to weight changes in healthy individuals of
             normal weight across a follow-up of over 20 y. PARTICIPANTS
             AND DESIGN: College students (3885 men and 841 women) were
             administered a self-report depression measure in the
             mid-1960s. Their baseline body mass index (BMI) was
             calculated from their college medical records. Participants
             were contacted by mail in the late 1980s and asked to report
             their current height and weight as well as their smoking and
             exercise habits. Another measure of depressive symptoms was
             obtained from 3560 individuals at follow-up. Multiple
             regression models were used to relate changes in weight to
             depression scores while controlling for background (gender,
             baseline BMI and the gender by BMI interaction) and
             behavioral (exercise and smoking) predictors. RESULTS: The
             relationship between depressive symptoms and body weight
             change took the form of an interaction with baseline BMI (P
             < 0.001). Those with high baseline depression scores gained
             less weight than their nondepressed counterparts if they
             were initially lean, but more if they were initially heavy.
             This trend was especially strong in those with high
             depression scores at both baseline and follow-up.
             CONCLUSIONS: The findings support the hypothesis that
             depression exaggerates pre-existing weight change
             tendencies. This pattern would not have been detected by an
             examination of main effects alone, illustrating the need to
             move toward more complicated interactive models in the study
             of psychological factors and weight.},
   Key = {fds141670}
}

@article{fds276436,
   Author = {R.S. Surwit and Barefoot, JC and Heitmann, BL and Helms, MJ and Williams, RB and Surwit,
             RS and Siegler, IC},
   Title = {Symptoms of depression and changes in body weight from
             adolescence to mid-life.},
   Journal = {Int J Obes Relat Metab Disord},
   Volume = {22},
   Number = {7},
   Pages = {688-694},
   Year = {1998},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9705031},
   Abstract = {OBJECTIVE: To investigate the relationship of symptoms of
             depression to weight changes in healthy individuals of
             normal weight across a follow-up of over 20 y. PARTICIPANTS
             AND DESIGN: College students (3885 men and 841 women) were
             administered a self-report depression measure in the
             mid-1960s. Their baseline body mass index (BMI) was
             calculated from their college medical records. Participants
             were contacted by mail in the late 1980s and asked to report
             their current height and weight as well as their smoking and
             exercise habits. Another measure of depressive symptoms was
             obtained from 3560 individuals at follow-up. Multiple
             regression models were used to relate changes in weight to
             depression scores while controlling for background (gender,
             baseline BMI and the gender by BMI interaction) and
             behavioral (exercise and smoking) predictors. RESULTS: The
             relationship between depressive symptoms and body weight
             change took the form of an interaction with baseline BMI (P
             < 0.001). Those with high baseline depression scores gained
             less weight than their nondepressed counterparts if they
             were initially lean, but more if they were initially heavy.
             This trend was especially strong in those with high
             depression scores at both baseline and follow-up.
             CONCLUSIONS: The findings support the hypothesis that
             depression exaggerates pre-existing weight change
             tendencies. This pattern would not have been detected by an
             examination of main effects alone, illustrating the need to
             move toward more complicated interactive models in the study
             of psychological factors and weight.},
   Doi = {10.1038/sj.ijo.0800647},
   Key = {fds276436}
}

@article{fds276437,
   Author = {R.S. Surwit and Surwit, RS and Wang, S and Petro, AE and Sanchis, D and Raimbault, S and Ricquier, D and Collins, S},
   Title = {Diet-induced changes in uncoupling proteins in obesity-prone
             and obesity-resistant strains of mice.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {95},
   Number = {7},
   Pages = {4061-4065},
   Year = {1998},
   Month = {March},
   ISSN = {0027-8424},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9520493},
   Abstract = {Uncoupling protein 2 (UCP2) maps to a region on distal mouse
             chromosome 7 that has been linked to the phenotypes of
             obesity and type II diabetes. We recently reported that UCP2
             expression is increased by high fat feeding in adipose
             tissue of the A/J strain of mice, which is resistant to the
             development of dietary obesity. More recently, a third UCP
             (UCP3) was identified, which is expressed largely in
             skeletal muscle and brown adipose tissue. The UCP2 and UCP3
             genes are located adjacent to one another on mouse
             chromosome 7. Thus, the roles of these UCPs in both
             metabolic efficiency and the linkage to obesity and diabetes
             syndromes is unclear. For this reason, we examined the
             expression of UCP2 and UCP3 in white adipose tissue and
             interscapular brown adipose tissue and in
             gastrocnemius/soleus muscle preparations from the
             obesity-resistant A/J and C57BL/KsJ (KsJ) strains and the
             obesity-prone C57BL/6J (B6) mouse strain. In both KsJ and
             A/J mice, UCP2 expression in white fat was increased
             approximately 2-fold in response to 2 weeks of a high fat
             diet, but there was no effect of diet on UCP2 levels in B6
             mice. In skeletal muscle and in brown fat, neither UCP2 nor
             UCP3 expression was affected by diet in A/J, B6, or KsJ
             mice. However, in brown fat, we observed a 2-3-fold increase
             in the expression of UCP1 in response to dietary fat
             challenge, which may be related to diet-induced elevations
             in plasma leptin levels. Together, these results indicate
             that the consumption of a high fat diet selectively
             regulates UCP2 expression in white fat and UCP1 expression
             in brown fat and that resistance to obesity is correlated
             with this early, selective induction of UCP1 and UCP2 and is
             not associated with changes in expression of
             UCP3.},
   Doi = {10.1073/pnas.95.7.4061},
   Key = {fds276437}
}

@article{fds305786,
   Author = {Surwit, RS},
   Title = {Sucrose in weight-loss regimens - Reply},
   Journal = {American Journal of Clinical Nutrition},
   Volume = {67},
   Number = {1},
   Pages = {151-151},
   Publisher = {AMER SOC CLINICAL NUTRITION},
   Year = {1998},
   Month = {January},
   ISSN = {0002-9165},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000071362100030&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305786}
}

@article{fds319714,
   Author = {SURWIT, RS},
   Title = {Diet-induced changes in uncoupling proteins in obesity-prone
             and obesity-resistant strains of mice},
   Journal = {Proc. Natl. Acad. Sci. Usa},
   Volume = {95},
   Number = {7},
   Pages = {4061-4065},
   Year = {1998},
   ISSN = {0027-8424},
   Keywords = {Adipose Tissue • Animals • Carrier Proteins •
             Chromosome Mapping • Diet* • Gene Expression
             Regulation • Ion Channels • Male • Membrane
             Transport Proteins* • Mice • Mitochondrial
             Proteins* • Molecular Sequence Data • Obesity
             • Protein Biosynthesis* • Proteins •
             biosynthesis* • genetics • metabolism*},
   Abstract = {Uncoupling protein 2 (UCP2) maps to a region on distal mouse
             chromosome 7 that has been linked to the phenotypes of
             obesity and type II diabetes. We recently reported that UCP2
             expression is increased by high fat feeding in adipose
             tissue of the A/J strain of mice, which is resistant to the
             development of dietary obesity. More recently, a third UCP
             (UCP3) was identified, which is expressed largely in
             skeletal muscle and brown adipose tissue. The UCP2 and UCP3
             genes are located adjacent to one another on mouse
             chromosome 7. Thus, the roles of these UCPs in both
             metabolic efficiency and the linkage to obesity and diabetes
             syndromes is unclear. For this reason, we examined the
             expression of UCP2 and UCP3 in white adipose tissue and
             interscapular brown adipose tissue and in
             gastrocnemius/soleus muscle preparations from the
             obesity-resistant A/J and C57BL/KsJ (KsJ) strains and the
             obesity-prone C57BL/6J (B6) mouse strain. In both KsJ and
             A/J mice, UCP2 expression in white fat was increased
             approximately 2-fold in response to 2 weeks of a high fat
             diet, but there was no effect of diet on UCP2 levels in B6
             mice. In skeletal muscle and in brown fat, neither UCP2 nor
             UCP3 expression was affected by diet in A/J, B6, or KsJ
             mice. However, in brown fat, we observed a 2-3-fold increase
             in the expression of UCP1 in response to dietary fat
             challenge, which may be related to diet-induced elevations
             in plasma leptin levels. Together, these results indicate
             that the consumption of a high fat diet selectively
             regulates UCP2 expression in white fat and UCP1 expression
             in brown fat and that resistance to obesity is correlated
             with this early, selective induction of UCP1 and UCP2 and is
             not associated with changes in expression of
             UCP3.},
   Key = {fds319714}
}

@article{fds141657,
   Author = {RS Surwit and AE Petro and P Parekh and S Collins},
   Title = {Low plasma leptin in response to dietary fat in diabetes-
             and obesity-prone mice.},
   Journal = {Diabetes, UNITED STATES},
   Volume = {46},
   Number = {9},
   Pages = {1516-20},
   Year = {1997},
   Month = {September},
   ISSN = {0012-1797},
   Keywords = {Animals • Body Temperature • Body Weight •
             Diabetes Mellitus, Experimental • Dietary Fats •
             Ion Channels • Leptin • Membrane Transport
             Proteins* • Mice • Mice, Inbred A • Mice,
             Inbred C57BL • Mice, Inbred Strains •
             Mitochondrial Proteins* • Obesity • Proteins
             • Time Factors • genetics • metabolism*
             • physiopathology*},
   Abstract = {Despite the fact that mutations resulting in the absence of
             leptin or its receptor have been associated with severe
             obesity and diabetes, such mutations do not appear to be
             responsible for most human obesity. Indeed, diet-induced
             obesity in animals and humans has been characterized by
             hyperleptinemia. This has been interpreted as evidence for
             leptin resistance. However, no careful longitudinal studies
             evaluating the role of leptin in the development of obesity
             exist. We report a series of studies in A/J and C57BL/6J
             (B/6) mice that demonstrate a direct relationship between
             the ability to increase plasma leptin levels in response to
             a high-fat diet and resistance to the subsequent development
             of obesity and diabetes. While leptin levels are similar in
             lean, low-fat-fed A/J and B/6 mice, the effects of a
             high-fat diet on plasma leptin differ dramatically between
             the two strains. After 4 weeks of high-fat feeding, leptin
             levels in A/J mice increased 10-fold, and this elevated
             level was maintained independent of weight gain throughout a
             14-week feeding period. However, in B/6 mice, leptin levels
             remained at least twofold lower and only rose very gradually
             along with a significant increase in adiposity,
             hyperglycemia, and hyperinsulinemia. These differences in
             the response of leptin to diet are independent of food
             intake and plasma insulin levels during the 1st month of
             feeding. Further, we demonstrated that leptin administration
             did not influence the expression of the novel uncoupling
             protein UCP2, which also responds to dietary fat. From these
             results, we suggest that the response of leptin to fat
             feeding may be an important predictor of the development of
             subsequent obesity.},
   Key = {fds141657}
}

@article{fds276438,
   Author = {R.S. Surwit and Surwit, RS and Petro, AE and Parekh, P and Collins,
             S},
   Title = {Low plasma leptin in response to dietary fat in diabetes-
             and obesity-prone mice.},
   Journal = {Diabetes},
   Volume = {46},
   Number = {9},
   Pages = {1516-1520},
   Year = {1997},
   Month = {September},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9287057},
   Abstract = {Despite the fact that mutations resulting in the absence of
             leptin or its receptor have been associated with severe
             obesity and diabetes, such mutations do not appear to be
             responsible for most human obesity. Indeed, diet-induced
             obesity in animals and humans has been characterized by
             hyperleptinemia. This has been interpreted as evidence for
             leptin resistance. However, no careful longitudinal studies
             evaluating the role of leptin in the development of obesity
             exist. We report a series of studies in A/J and C57BL/6J
             (B/6) mice that demonstrate a direct relationship between
             the ability to increase plasma leptin levels in response to
             a high-fat diet and resistance to the subsequent development
             of obesity and diabetes. While leptin levels are similar in
             lean, low-fat-fed A/J and B/6 mice, the effects of a
             high-fat diet on plasma leptin differ dramatically between
             the two strains. After 4 weeks of high-fat feeding, leptin
             levels in A/J mice increased 10-fold, and this elevated
             level was maintained independent of weight gain throughout a
             14-week feeding period. However, in B/6 mice, leptin levels
             remained at least twofold lower and only rose very gradually
             along with a significant increase in adiposity,
             hyperglycemia, and hyperinsulinemia. These differences in
             the response of leptin to diet are independent of food
             intake and plasma insulin levels during the 1st month of
             feeding. Further, we demonstrated that leptin administration
             did not influence the expression of the novel uncoupling
             protein UCP2, which also responds to dietary fat. From these
             results, we suggest that the response of leptin to fat
             feeding may be an important predictor of the development of
             subsequent obesity.},
   Doi = {10.2337/diab.46.9.1516},
   Key = {fds276438}
}

@article{fds141639,
   Author = {RS Surwit and MN Feinglos and CC McCaskill and SL Clay and MA Babyak and BS
             Brownlow, CS Plaisted and PH Lin},
   Title = {Metabolic and behavioral effects of a high-sucrose diet
             during weight loss.},
   Journal = {The American journal of clinical nutrition, UNITED
             STATES},
   Volume = {65},
   Number = {4},
   Pages = {908-15},
   Year = {1997},
   Month = {April},
   ISSN = {0002-9165},
   Keywords = {Adult • Analysis of Variance • Behavior •
             Blood Glucose • Blood Pressure • Body Composition
             • Body Mass Index • Body Weight • Cholesterol
             • Diet, Fat-Restricted • Dietary Sucrose •
             Energy Metabolism • Epinephrine • Female •
             Humans • Lipids • Middle Aged • Thyrotropin
             • Thyroxine • Triiodothyronine • Weight Loss
             • analysis • blood • drug effects •
             pharmacology* • physiology • physiology*},
   Abstract = {In response to evidence linking obesity and high amounts of
             dietary fat, the food industry has developed numerous
             reduced-fat and nonfat food items. These items frequently
             derive a relatively large percentage of their energy from
             sugars and the effect of these sugars on weight regulation
             is not well known. We studied the comparative effects of
             high- and low-sucrose, low-fat, hypoenergetic diets on a
             variety of metabolic and behavioral indexes in a 6-wk
             weight-loss program. Both diets contained approximately 4606
             kJ energy/d with 11% of energy as fat, 19% as protein, and
             71% as carbohydrate. The high-sucrose diet contained 43% of
             the total daily energy intake as sucrose; the low-sucrose
             diet contained 4% of the total daily energy intake as
             sucrose. Twenty women aged 40.6 +/- 8.2 y (mean +/- SD) with
             a body mass index (in kg/m2) of 35.93 +/- 4.8 consumed the
             high-sucrose diet; 22 women aged 40.3 +/- 7.3 y with a body
             mass index of 34.93 +/- 4.4 consumed the low-sucrose diet.
             Mixed-design analysis of variance showed a main effect of
             time (P < 0.01), with both diet groups showing decreases in
             weight, blood pressure, resting energy expenditure,
             percentage body fat, free triiodothyronine (FT3), urinary
             norepinephrine, and plasma lipids. Small but significant
             interactions were found between group and time in total
             cholesterol (P = 0.009) and low-density lipoprotein (LDL) (P
             = 0.01). Both groups showed decreases in depression, hunger,
             and negative mood, and increases in vigilance and positive
             mood with time (P < 0.01). Results showed that a high
             sucrose content in a hypoenergetic, low-fat diet did not
             adversely affect weight loss, metabolism, plasma lipids, or
             emotional affect.},
   Key = {fds141639}
}

@article{fds276440,
   Author = {R.S. Surwit and Surwit, RS and Feinglos, MN and McCaskill, CC and Clay, SL and Babyak,
             MA and Brownlow, BS and Plaisted, CS and Lin, PH},
   Title = {Metabolic and behavioral effects of a high-sucrose diet
             during weight loss.},
   Journal = {American Journal of Clinical Nutrition},
   Volume = {65},
   Number = {4},
   Pages = {908-915},
   Year = {1997},
   Month = {April},
   ISSN = {0002-9165},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9094871},
   Abstract = {In response to evidence linking obesity and high amounts of
             dietary fat, the food industry has developed numerous
             reduced-fat and nonfat food items. These items frequently
             derive a relatively large percentage of their energy from
             sugars and the effect of these sugars on weight regulation
             is not well known. We studied the comparative effects of
             high- and low-sucrose, low-fat, hypoenergetic diets on a
             variety of metabolic and behavioral indexes in a 6-wk
             weight-loss program. Both diets contained approximately 4606
             kJ energy/d with 11% of energy as fat, 19% as protein, and
             71% as carbohydrate. The high-sucrose diet contained 43% of
             the total daily energy intake as sucrose; the low-sucrose
             diet contained 4% of the total daily energy intake as
             sucrose. Twenty women aged 40.6 +/- 8.2 y (mean +/- SD) with
             a body mass index (in kg/m2) of 35.93 +/- 4.8 consumed the
             high-sucrose diet; 22 women aged 40.3 +/- 7.3 y with a body
             mass index of 34.93 +/- 4.4 consumed the low-sucrose diet.
             Mixed-design analysis of variance showed a main effect of
             time (P < 0.01), with both diet groups showing decreases in
             weight, blood pressure, resting energy expenditure,
             percentage body fat, free triiodothyronine (FT3), urinary
             norepinephrine, and plasma lipids. Small but significant
             interactions were found between group and time in total
             cholesterol (P = 0.009) and low-density lipoprotein (LDL) (P
             = 0.01). Both groups showed decreases in depression, hunger,
             and negative mood, and increases in vigilance and positive
             mood with time (P < 0.01). Results showed that a high
             sucrose content in a hypoenergetic, low-fat diet did not
             adversely affect weight loss, metabolism, plasma lipids, or
             emotional affect.},
   Doi = {10.1093/ajcn/65.4.908},
   Key = {fds276440}
}

@article{fds276357,
   Author = {Fleury, C and Neverova, M and Collins, S and Raimbault, S and Champigny,
             O and Levi-Meyrueis, C and Bouillaud, F and Seldin, MF and Surwit, RS and Ricquier, D and Warden, CH},
   Title = {Uncoupling protein-2: a novel gene linked to obesity and
             hyperinsulinemia.},
   Journal = {Nature Genetics},
   Volume = {15},
   Number = {3},
   Pages = {269-272},
   Year = {1997},
   Month = {March},
   ISSN = {1061-4036},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9054939},
   Keywords = {Adipose Tissue • Adipose Tissue, Brown • Adult
             • Animals • Base Sequence • Carrier Proteins
             • Chromosome Mapping* • Chromosomes, Human, Pair
             11* • DNA Primers • Diabetes Mellitus •
             Humans • Hyperinsulinism • Ion Channels •
             Membrane Proteins • Membrane Transport Proteins* •
             Mice • Mitochondrial Proteins* • Models,
             Biological • Molecular Sequence Data • Obesity
             • Organ Specificity • Polymerase Chain Reaction
             • Proteins* • Up-Regulation • biosynthesis
             • genetics • genetics* • metabolism •
             metabolism*},
   Abstract = {A mitochondrial protein called uncoupling protein (UCP1)
             plays an important role in generating heat and burning
             calories by creating a pathway that allows dissipation of
             the proton electrochemical gradient across the inner
             mitochondrial membrane in brown adipose tissue, without
             coupling to any other energy-consuming process. This pathway
             has been implicated in the regulation of body temperature,
             body composition and glucose metabolism. However,
             UCP1-containing brown adipose tissue is unlikely to be
             involved in weight regulation in adult large-size animals
             and humans living in a thermoneutral environment (one where
             an animal does not have to increase oxygen consumption or
             energy expenditure to lose or gain heat to maintain body
             temperature), as there is little brown adipose tissue
             present. We now report the discovery of a gene that codes
             for a novel uncoupling protein, designated UCP2, which has
             59% amino-acid identity to UCP1, and describe properties
             consistent with a role in diabetes and obesity. In
             comparison with UCP1, UCP2 has a greater effect on
             mitochondrial membrane potential when expressed in yeast.
             Compared to UCP1, the gene is widely expressed in adult
             human tissues, including tissues rich in macrophages, and it
             is upregulated in white fat in response to fat feeding.
             Finally, UCP2 maps to regions of human chromosome 11 and
             mouse chromosome 7 that have been linked to
             hyperinsulinaemia and obesity. Our findings suggest that
             UCP2 has a unique role in energy balance, body weight
             regulation and thermoregulation and their responses to
             inflammatory stimuli.},
   Doi = {10.1038/ng0397-269},
   Key = {fds276357}
}

@article{fds276316,
   Author = {Surwit, R and Petro, AE and Parekh, P and Collins,
             S},
   Title = {Erratum: Low plasma leptin in response to dietary fat in
             diabetes- and obesity-prone mice (Diabetes (1997) 46
             (1516-1520))},
   Journal = {Diabetes},
   Volume = {46},
   Number = {11},
   Pages = {1920},
   Year = {1997},
   Month = {January},
   Key = {fds276316}
}

@article{fds276407,
   Author = {Collins, S and Daniel, KW and Petro, AE and Surwit,
             RS},
   Title = {Strain-specific response to beta 3-adrenergic receptor
             agonist treatment of diet-induced obesity in
             mice.},
   Journal = {Endocrinology},
   Volume = {138},
   Number = {1},
   Pages = {405-413},
   Year = {1997},
   Month = {January},
   ISSN = {0013-7227},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8977430},
   Keywords = {Adipocytes • Adrenergic beta-Agonists • Animals
             • Blood Glucose • Carrier Proteins • Dietary
             Fats • Insulin • Ion Channels • Male •
             Membrane Proteins • Mice • Mitochondrial Proteins
             • Obesity • RNA, Messenger • Receptors,
             Adrenergic, beta • Receptors, Adrenergic, beta-3 •
             Species Specificity • adverse effects* • analysis
             • blood • genetics • pharmacology* •
             physiology* • physiopathology*},
   Abstract = {Fat intake has long been associated with the development of
             obesity. The studies described herein show that fat
             adversely affects adipocyte adrenergic receptor (AR)
             expression and function. As beta 3AR agonists have been
             shown to acutely reduce adipose tissue mass and improve
             thermogenesis in genetically obese rodents, we examined
             whether chronic supplementation of a high fat diet with a
             highly selective beta 3AR agonist, CL316,243 could prevent
             diet-induced obesity, and whether the effect could be
             sustained over prolonged treatment. C57BL/6J and A/J mice
             were weaned onto one of three diets: low fat (10.5% calories
             from fat), high fat (58% calories from fat), or high fat
             supplemented with 0.001% CL316,243. B/6J mice gained more
             weight on the high fat diet than A/J mice (at 16 weeks:
             B/6J, 36.6 +/- 1.4 g; A/J, 32.9 +/- 0.8 g; P < 0.002; n =
             10), whereas weights on the low fat diets were similar
             (B/6J, 29.5 +/- 0.5 g; A/J, 28.8 +/- 0.6 g; P > 0.05; n =
             10). CL316,243 prevented the development of diet-induced
             obesity in A/J animals, but not in B/6J animals. A/J mice
             weighed 26.0 +/- 0.5 g at 16 weeks, whereas B/6J animals on
             the same diet weighed 34.1 +/- 0.8 g (P < 0.00001; n = 10),
             but food intake was not different between the strains
             throughout the study. beta-Adrenergic stimulation of
             adenylyl cyclase in obese B/6J mice was decreased by more
             than 75% in white adipose tissue and by more than 90% in
             brown adipose tissue (BAT). In contrast, in fat-fed A/J
             mice, beta-agonist-stimulated adenylyl cyclase was decreased
             in white adipose tissue by about 10%, whereas the activity
             in interscapular BAT was decreased by 50%, indicating
             significant retention of beta AR-stimulated activity in A/J
             mice compared to B/6J mice. High fat feeding was associated
             with decreased expression of beta 3AR and beta 1AR in white
             adipose tissue of both strains. However, chronic CL316,243
             treatment prevented both the obesity and the decline in beta
             3AR and beta 1AR messenger RNA levels in all adipose depots
             from A/J mice, but not B/6J mice. As CL316,243-treated A/J
             mice, but not B/6J mice, also showed marked uncoupling
             protein expression in white adipose depots, the ability of
             chronic CL316,243 treatment to prevent diet-induced obesity
             is dependent upon the elaboration of functional BAT in these
             regions.},
   Doi = {10.1210/endo.138.1.4829},
   Key = {fds276407}
}

@article{fds141566,
   Title = {Surwit RS, Petro AE, Parekh P, Collins S: Low plasma leptin
             in response to dietary fat in diabetes and obesity prone
             mice. Diabetes 46: 1516-1520, 1997.},
   Year = {1997},
   Key = {fds141566}
}

@article{fds141606,
   Title = {Fleury C, Neverova M, Collins S, Raimbault S, Champign O,
             Levi Meyrueis C, Bouillaud F, Seldin MF, Surwit RS, ricquier
             D, Warden CH: Uncoupling protein-2: A novel candidate
             thermogenic protein linked to obesity and insulin
             resistance. Nature Genetics 15: 269-272,
             1997.},
   Year = {1997},
   Key = {fds141606}
}

@article{fds141615,
   Title = {Collins S, Daniel KW, Petro AE, Surwit RS: Strain-specific
             response to B3 AR agonist treatment of diet-induced obesity
             in mice. Endocrinology 138: 405-413, 1997.},
   Year = {1997},
   Key = {fds141615}
}

@article{fds141616,
   Title = {Surwit RS, Feinglos MN, McCaskill CC, Clay SL, Babyak MA,
             Brownlow BS, Plaisted CG, Lin PH: Metabolic and behavioral
             effects of a high sucrose diet in weight loss. American
             Journal Clinical Nutrition 65: 908-915, 1997.},
   Year = {1997},
   Key = {fds141616}
}

@article{fds141617,
   Title = {Fleury C, Neverova M, Collins S, Raimbault S, Champign O,
             Levi-Meyrueis C, Bouillaud F, Seldin MF, Surwit RS, Ricquier
             D, Warden CH: Uncompling protein-2: A novel candidate
             thermogenic protein linked to obesity and insulin
             resistance. Nature Genetics 15: 269-272,
             1997.},
   Year = {1997},
   Key = {fds141617}
}

@article{fds276439,
   Author = {R.S. Surwit and Fleury, C and Neverova, M and Collins, S and Raimbault, S and Champign,
             O and Levi Meyrueis and C and Bouillaud, F and Seldin, MF and Ricquier, D and Warden, CH},
   Title = {Uncoupling protein-2: A novel candidate thermogenic protein
             linked to obesity and insulin resistance},
   Journal = {Nature Genetics},
   Volume = {15},
   Pages = {269-272},
   Year = {1997},
   Key = {fds276439}
}

@article{fds141579,
   Author = {BS Brownlow and A Petro and MN Feinglos and RS Surwit},
   Title = {The role of motor activity in diet-induced obesity in
             C57BL/6J mice.},
   Journal = {Physiology & behavior, UNITED STATES},
   Volume = {60},
   Number = {1},
   Pages = {37-41},
   Year = {1996},
   Month = {July},
   ISSN = {0031-9384},
   Keywords = {Animals • Blood Glucose • Dietary Fats •
             Energy Intake • Insulin • Male • Mice •
             Mice, Inbred A • Mice, Inbred C57BL • Mice, Obese
             • Motor Activity • Obesity • Species
             Specificity • Weight Gain • administration &
             dosage* • blood • genetics • genetics* •
             metabolism • physiology},
   Abstract = {Previous research in our laboratory has demonstrated that
             the C57BL/6J (B/6J) mouse has a predisposition to develop
             severe obesity if placed on a high-fat diet. In the present
             study we assessed the role of physical activity in this
             phenomenon. Obesity-prone B/6J and obesity-resistant A/J
             mice were placed on one of four diets; high fat/high
             sucrose, high fat/low sucrose, low fat/high sucrose, and low
             fat/low sucrose. After 4 months, all animals on the high-fat
             diets had gained more weight than animals on the low-fat
             diets, and this phenomenon was greatly exaggerated in B/6J
             mice. Despite the fact that B/6J mice gained more weight
             than A/J mice on high-fat diets without consuming more
             calories, spontaneous motor activity was elevated in B/6J
             mice compared to A/J mice. There was no effect of the diets
             on activity either within or across strains. These data
             suggest that predisposition to diet-induced obesity is not
             explainable by reduced levels of physical
             activity.},
   Key = {fds141579}
}

@article{fds276442,
   Author = {R.S. Surwit and Brownlow, BS and Petro, A and Feinglos, MN and Surwit,
             RS},
   Title = {The role of motor activity in diet-induced obesity in
             C57BL/6J mice.},
   Journal = {Physiology & Behavior},
   Volume = {60},
   Number = {1},
   Pages = {37-41},
   Year = {1996},
   Month = {July},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8804640},
   Abstract = {Previous research in our laboratory has demonstrated that
             the C57BL/6J (B/6J) mouse has a predisposition to develop
             severe obesity if placed on a high-fat diet. In the present
             study we assessed the role of physical activity in this
             phenomenon. Obesity-prone B/6J and obesity-resistant A/J
             mice were placed on one of four diets; high fat/high
             sucrose, high fat/low sucrose, low fat/high sucrose, and low
             fat/low sucrose. After 4 months, all animals on the high-fat
             diets had gained more weight than animals on the low-fat
             diets, and this phenomenon was greatly exaggerated in B/6J
             mice. Despite the fact that B/6J mice gained more weight
             than A/J mice on high-fat diets without consuming more
             calories, spontaneous motor activity was elevated in B/6J
             mice compared to A/J mice. There was no effect of the diets
             on activity either within or across strains. These data
             suggest that predisposition to diet-induced obesity is not
             explainable by reduced levels of physical
             activity.},
   Doi = {10.1016/0031-9384(95)02210-4},
   Key = {fds276442}
}

@article{fds276372,
   Author = {Collins, S and Kuhn, CM and Petro, AE and Swick, AG and Chrunyk, BA and Surwit, RS},
   Title = {Role of leptin in fat regulation.},
   Journal = {Nature},
   Volume = {380},
   Number = {6576},
   Pages = {677},
   Year = {1996},
   Month = {April},
   ISSN = {0028-0836},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8614460},
   Keywords = {Adipose Tissue • Adipose Tissue, Brown • Animals
             • Body Temperature Regulation • Body Weight •
             Catecholamines • Eating • Enzyme Inhibitors •
             Female • Leptin • Methyltyrosines • Mice
             • Mice, Inbred C57BL • Norepinephrine •
             Obesity • Proteins • Sympathetic Nervous System
             • Tyrosine 3-Monooxygenase • alpha-Methyltyrosine
             • antagonists & inhibitors • etiology •
             metabolism • pharmacology • physiology •
             physiology*},
   Doi = {10.1038/380677a0},
   Key = {fds276372}
}

@article{fds276423,
   Author = {Collins, S and Surwit, RS},
   Title = {Pharmacologic manipulation of ob expression in a dietary
             model of obesity.},
   Journal = {The Journal of Biological Chemistry},
   Volume = {271},
   Number = {16},
   Pages = {9437-9440},
   Year = {1996},
   Month = {April},
   ISSN = {0021-9258},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8621612},
   Keywords = {Adipose Tissue • Adipose Tissue, Brown •
             Adrenergic beta-Agonists • Animals • Base Sequence
             • Blotting, Northern • DNA Primers • Dietary
             Fats • Dioxoles • Energy Intake • Gene
             Expression* • Leptin • Male • Mice •
             Mice, Inbred A • Mice, Inbred C57BL • Mice, Obese
             • Molecular Sequence Data • Obesity • Organ
             Specificity • Polymerase Chain Reaction • Protein
             Biosynthesis* • Proteins • RNA, Messenger •
             Species Specificity • biosynthesis • drug effects
             • genetics • genetics* • pharmacology •
             physiopathology*},
   Abstract = {Mutation of the obese (ob) gene results in severe hereditary
             obesity and diabetes in the C57BL/6J and related strains of
             mice. In this study we examined the expression of the ob
             gene in a dietary model in which moderate obesity develops
             in response to fat (58% of calories from fat) without
             mutation of the ob gene, and in four genetic models of
             obesity in mice: ob/ob, db/db, tubby, and fat. Several white
             and brown adipose depots were examined (epididymal,
             subcutaneous, perirenal, and interscapular). Northern blot
             analysis shows that levels of ob mRNA are increased in all
             adipose depots examined in every model of obesity. The
             average fold increases were 12.0 +/ 2.1 (ob/ob), 4.8 +/- 1.5
             (db/db), 2.8 +/- 0.1 (tubby), 2.4 +/- 0.3 (fat), and 2.1 +/-
             0.2 (high fat diet-induced A/J). Moreover, we found that the
             expression of the ob gene could be manipulated by
             pharmacologically blocking the development of diet-induced
             obesity. Supplementation of a high fat diet with a beta
             3-adrenergic receptor agonist (CL316,243) prevented obesity,
             but not hyperphagia associated with high fat feeding (body
             weights of high fat-fed A/J mice = 34.0 +/- 1.0 g; high fat
             plus CL316,243-fed mice = 26.8 +/- 0.5 g; n = 10).
             CL316,243-treated, high fat-fed animals contained levels of
             ob mRNA in all adipose depots that were equal to or less
             than levels in low fat-fed mice (average levels in high fat
             plus CL316,243-fed mice relative to low fat-fed mice: 0.93
             +/- 0.09). Inasmuch as fat cell size, but not number, was
             increased in a previous study in diet-induced obese A/J
             mice, these results indicate that expression of the ob gene
             serves as a sensor of fat cell hypertrophy, independent of
             any effects on food intake.},
   Doi = {10.1074/jbc.271.16.9437},
   Key = {fds276423}
}

@article{fds276361,
   Author = {Opara, EC and Petro, A and Tevrizian, A and Feinglos, MN and Surwit,
             RS},
   Title = {L-glutamine supplementation of a high fat diet reduces body
             weight and attenuates hyperglycemia and hyperinsulinemia in
             C57BL/6J mice.},
   Journal = {The Journal of Nutrition},
   Volume = {126},
   Number = {1},
   Pages = {273-279},
   Year = {1996},
   Month = {January},
   ISSN = {0022-3166},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8558312},
   Keywords = {Animals • Blood Glucose • Body Weight •
             Dietary Carbohydrates • Dietary Fats • Eating
             • Fatty Acids • Food, Fortified • Glutamine
             • Hyperglycemia • Hyperinsulinism • Insulin
             • Insulin Resistance • Lipids • Male •
             Mice • Mice, Inbred C57BL • Obesity •
             Oxidation-Reduction • administration & dosage •
             administration & dosage* • analysis • blood •
             diet therapy* • drug effects • metabolism •
             pharmacology • pharmacology* • physiology •
             physiopathology • standards},
   Abstract = {C57BL/6J (B/6J) mice are genetically predisposed to become
             overweight and develop hyperglycemia if raised on a high fat
             diet. The purpose of the present study was to explore the
             effect of dietary supplementation of L-glutamine (Gln), an
             inhibitor of fatty acid oxidation, on the development of
             hyperglycemia and excessive weight gain. Groups of 10 age-
             and weight-matched male B/6J mice were raised on one of four
             diets: 1) a low fat, low sucrose (LL), studied separately,
             2) a high fat, low sucrose (HL) diet alone, 3) high fat, low
             sucrose supplemented with L-glutamine (HL+Gln) and 4) high
             fat, low sucrose supplemented with L-alanine (HL+Ala).
             Energy intake, body weight, plasma glucose and insulin
             concentrations were monitored over time. We found no
             difference in energy intake per unit body weight between any
             groups after the first 2 wk of feeding. However, the mean
             +/- SEM for body weight (27.1 +/- 0.6 g) of the LL group
             measured at 16 wk was lower (P < 0.05) than that of the HL
             group at 37.9 +/- 1.9 g. Also, after 5.5 mo, the mean +/-
             SEM for plasma glucose and insulin concentrations in the LL
             group of mice were 6.9 +/- 0.4 mmol/l and 146 +/- 30 pmol/l,
             which were lower (P < 0.05) than those in the HL group at
             10.1 +/- 0.9 mmol/l and 438 +/- 84 pmol/l, respectively.
             Although both amino acids caused a 10% reduction (P < 0.05)
             in body weight compared with HL feeding at wk 16, only Gln
             supplementation resulted in persistent reductions in both
             plasma glucose and insulin concentrations over 5.5 mo. In
             another experiment, when Gln was added to the high fat (HL)
             diet of heavy hyperglycemic animals for 2 mo, body weight
             gain, hyperglycemia and hyperinsulinemia were attenuated. In
             conclusion, supplementing glutamine to a high fat diet
             reduces body weight and attenuated hyperglycemia and
             hyperinsulinemia in B/6J mice.},
   Doi = {10.1093/jn/126.1.273},
   Key = {fds276361}
}

@article{fds141559,
   Title = {Collins S, Kuhn CM, Petro AE, Swick AG, Chruny BA, Surwit
             RS: Role of leptin in fat regulation. Nature 360: 677,
             1996.},
   Year = {1996},
   Key = {fds141559}
}

@article{fds141564,
   Title = {Collins S, Kuhn CM, Petro AE, Swick AG, Chruny BA, Surwit
             RS: Role of leptin in fat regulation Nature 380: 677,
             1996.},
   Year = {1996},
   Key = {fds141564}
}

@article{fds141565,
   Title = {Surwit RS, Williams P: Animal models provide insight into
             psychosomatic factors in diabetes. Psychosomatic Medicine
             58: 582-589, 1996.},
   Year = {1996},
   Key = {fds141565}
}

@article{fds141604,
   Title = {Collins S, Surwit RS: Pharmacologic manipulation of ob
             expression in a dietary model of obesity. Journal of
             Biological Chemistry 271: 9437-9440, 1996.},
   Year = {1996},
   Key = {fds141604}
}

@article{fds141605,
   Title = {Brownlow BS, Petro A, Feinglos MN, Surwit RS: The role of
             motor activity in diet-induced obesity in C57BL/6J mice.
             Physiology and Behavior 60: 37-41, 1996.},
   Year = {1996},
   Key = {fds141605}
}

@article{fds141614,
   Title = {Opara EC, Petro AE, Tevrizian A, Feinglos MN, Surwit RS:
             Metabolic efficacy of L-glutamine supplementation during
             high fat feeding in the C57BL/6J mouse. the Journal of
             Nutrition 126: 273-279, 1996.},
   Year = {1996},
   Key = {fds141614}
}

@article{fds276382,
   Author = {Surwit, RS and Williams, PG},
   Title = {Animal models provide insight into psychosomatic factors in
             diabetes.},
   Journal = {Psychosomatic Medicine},
   Volume = {58},
   Number = {6},
   Pages = {582-589},
   Year = {1996},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8948006},
   Keywords = {Animals • Diabetes Mellitus • Disease Models,
             Animal* • Disease Susceptibility • Humans •
             Hyperphagia • Mice • Mice, Inbred Strains •
             Obesity • Psychophysiologic Disorders* • Stress
             • physiopathology • psychology •
             psychology*},
   Abstract = {OBJECTIVE: To review the literature regarding the use of
             animal models in research addressing psychosomatic aspects
             of diabetes. METHOD: We examine the key findings in animal
             model vs. human research in the area of stress and diabetes.
             Previous research has suggested that stress is a potential
             contributor to chronic hyperglycemia in diabetes. Stress
             affects metabolic activity via the stimulation of a variety
             of hormones that can result in elevated blood glucose
             levels. In patients with diabetes, due to a relative or
             absolute lack of insulin, stress-induced increases in
             glucose cannot be properly metabolized. Additionally,
             regulation of these stress hormones may be abnormal in
             diabetes. RESULTS: Human studies on the role of stress in
             the onset and course of type II diabetes are few and are
             limited by the constraints and logistics of examining life
             stress in humans. However, animal research allows for tight
             experimental control and the manipulation of factors that
             may contribute to the development and/or course of diabetes,
             such as stress, eating behavior, the nutrient content of
             food, and physical activity. Disease processes can be
             examined at a mechanistic level in animals which is
             typically limited in human research. CONCLUSIONS: There is a
             large body of animal work to support the notion that stress
             reliably produces hyperglycemia in type II diabetes.
             Furthermore, there is evidence that the autonomic nervous
             system plays a role in the pathophysiology of this condition
             in both animals and humans. Examination of eating behavior
             and nutrient content of food in animal models of diabetes
             has shed light on the role of these factors in the
             development of diabetes, as well as obesity. Finally,
             genetic research using animal models of diabetes will
             provide new directions for research in humans to delineate
             the genetic contribution to the development of
             diabetes.},
   Doi = {10.1097/00006842-199611000-00006},
   Key = {fds276382}
}

@article{fds276417,
   Author = {Lee, SK and Opara, EC and Surwit, RS and Feinglos, MN and Akwari,
             OE},
   Title = {Defective glucose-stimulated insulin release from perifused
             islets of C57BL/6J mice.},
   Journal = {Pancreas},
   Volume = {11},
   Number = {2},
   Pages = {206-211},
   Year = {1995},
   Month = {August},
   ISSN = {0885-3177},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7479681},
   Keywords = {Animals • Blood Glucose • Diabetes Mellitus,
             Experimental • Diabetes Mellitus, Type 2 • Dietary
             Carbohydrates • Dietary Fats • Glucose •
             Insulin • Islets of Langerhans • Lauric Acids
             • Male • Mice • Mice, Inbred C57BL •
             Perfusion • administration & dosage • drug effects
             • etiology • metabolism • pathology •
             pharmacology • pharmacology* •
             secretion*},
   Abstract = {Previous work has shown that the C57BL/6J (BL/6) mouse
             strain develops type 2 diabetes after being fed a high-fat,
             high-simple carbohydrate (HFHSC) diet. In contrast, the AJ
             mouse strain does not. The aim of the present study was to
             determine if differences in the insulin secretory
             characteristics of isolated perifused islets of these
             animals could help explain why the BL/6 mouse develops
             diet-induced diabetes. Insulin secretion was assessed as
             mean integrated area under the curve during 20 min of
             stimulation with 27.7 mM glucose or 5 mM lauric acid. We
             found that both glucose- and laurate-stimulated insulin
             secretions were significantly less in euglycemic BL/6 mice
             than in the euglycemic AJ mice. The defect in insulin
             response to glucose, but not laurate, in islets from the
             BL/6 mouse was exacerbated when the animals were fed the
             HFHSC diet. These data suggest that the BL/6 mouse has a
             defective insulin response to glucose, which is exacerbated
             by a diabetogenic diet.},
   Doi = {10.1097/00006676-199508000-00016},
   Key = {fds276417}
}

@article{fds276351,
   Author = {Wencel, HE and Smothers, C and Opara, EC and Kuhn, CM and Feinglos, MN and Surwit, RS},
   Title = {Impaired second phase insulin response of diabetes-prone
             C57BL/6J mouse islets.},
   Journal = {Physiology & Behavior},
   Volume = {57},
   Number = {6},
   Pages = {1215-1220},
   Year = {1995},
   Month = {June},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7652047},
   Keywords = {Animals • Diabetes Mellitus, Type 2 • Diet •
             Dietary Carbohydrates • Dietary Fats • Glucose
             • Insulin • Islets of Langerhans • Male
             • Mice • Mice, Inbred C57BL • Mice, Inbred
             Strains • Stimulation, Chemical • genetics •
             pharmacology • physiopathology* •
             secretion*},
   Abstract = {The C57BL/6J mouse develops obesity and diabetes in response
             to a high-fat, high-simple carbohydrate diet. To determine
             the dynamics of glucose-induced insulin release in this
             animal model of NIDDM, we studied the acute insulin response
             to glucose of perifused islets in C57BL/6J (diabetes-prone)
             and A/J (diabetes-resistant) mice fed a normal control diet
             and of others fed a diabetogenic diet. The insulin response
             of normal C57BL/6J islets was almost monophasic, with a
             deficiency in the second phase during high glucose
             stimulation when compared to that of A/J control islets. The
             defect in C57BL/6J mice was exaggerated in animals fed a
             diabetogenic diet. It is suggested that a latent deficiency
             of second phase insulin release may contribute to the
             development of the diet-induced syndrome in this
             model.},
   Doi = {10.1016/0031-9384(95)00022-b},
   Key = {fds276351}
}

@article{fds276374,
   Author = {Gettys, TW and Ramkumar, V and Surwit, RS and Taylor,
             IL},
   Title = {Tissue-specific alterations in G protein expression in
             genetic versus diet-induced models of non-insulin-dependent
             diabetes mellitus in the mouse.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {44},
   Number = {6},
   Pages = {771-778},
   Year = {1995},
   Month = {June},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7783662},
   Keywords = {Adipose Tissue • Animals • Diabetes Mellitus, Type
             2 • Diet* • GTP-Binding Proteins • Male
             • Mice • Mice, Inbred C57BL • Obesity •
             Reference Values • etiology • etiology* •
             genetics • genetics* • metabolism •
             metabolism*},
   Abstract = {Various tissues were obtained from the well-characterized
             genetic model (C57BL/6J-ob/ob) of non-insulin-dependent
             diabetes mellitus (NIDDM) and from a diet-induced model of
             NIDDM produced in the same genetic background (C57BL/6J).
             The objectives were to determine whether the previously
             observed changes in guanine nucleotide-binding regulatory
             protein (G protein) expression in adipose tissue from ob/ob
             mice were mirrored by concomitant changes in other tissues,
             and whether NIDDM of a different etiology would share
             similar alterations in G protein expression. Plasma
             membranes from adipocytes, brain, heart, liver, and testes
             were probed with alpha-subunit-specific antisera, and the
             level of G protein expression in each model was compared
             with that in its lean littermate control. Adipose, heart,
             and liver cell membranes from ob/ob mice contained
             significantly less alpha-subunit of stimulatory G protein
             (Gs alpha) than those from their lean littermates. As
             compared with the lean littermates, heart alpha-subunit-2 of
             inhibitory G protein (Gi alpha-2), liver Gi alpha-3, and
             adipocyte G1 alpha-1 and Gi alpha-3 were also reduced in
             ob/ob mice. In contrast, Gi alpha-2 and Go alpha were
             increased over lean-control levels in brain tissue from
             ob/ob mice, whereas Gs alpha was unchanged. G protein
             expression in the testes did not differ between lean and
             ob/ob mice. In the diet-induced model of NIDDM, Gs alpha
             expression in the liver was twofold greater in
             obese/diabetic mice as compared with lean controls. However,
             G protein expression in all other tissues examined did not
             differ between obese/diabetic animals and lean
             littermates.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Doi = {10.1016/0026-0495(95)90191-4},
   Key = {fds276374}
}

@article{fds276380,
   Author = {Edens, JL and Surwit, RS},
   Title = {In support of behavioral treatment for day wetting in
             children.},
   Journal = {Urology},
   Volume = {45},
   Number = {6},
   Pages = {905-908},
   Year = {1995},
   Month = {June},
   ISSN = {0090-4295},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7771021},
   Keywords = {Behavior Therapy* • Child • Enuresis •
             Exercise Therapy • Humans • methods •
             therapy*},
   Doi = {10.1016/s0090-4295(99)80106-x},
   Key = {fds276380}
}

@article{fds276354,
   Author = {Surwit, RS and Feinglos, MN and Rodin, J and Sutherland, A and Petro,
             AE and Opara, EC and Kuhn, CM and Rebuffé-Scrive,
             M},
   Title = {Differential effects of fat and sucrose on the development
             of obesity and diabetes in C57BL/6J and A/J
             mice.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {44},
   Number = {5},
   Pages = {645-651},
   Year = {1995},
   Month = {May},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7752914},
   Keywords = {Adipose Tissue • Analysis of Variance • Animals
             • Blood Glucose • Body Weight • Diabetes
             Mellitus • Dietary Carbohydrates • Dietary Fats
             • Energy Intake • Hyperplasia • Insulin
             • Male • Mice • Mice, Inbred A • Mice,
             Inbred C57BL • Obesity* • Organ Size •
             Sucrose • Weight Gain • anatomy & histology •
             blood • metabolism • pathology •
             pharmacology* • physiopathology*},
   Abstract = {We have previously demonstrated that the C57BL/6J (B/6J)
             mouse will develop severe obesity, hyperglycemia, and
             hyperinsulinemia if weaned onto a high-fat, high-sucrose
             (HH) diet. In the present study, we compared the effects of
             fat and sucrose separately and in combination on diabetes-
             and obesity-prone B/6J and diabetes- and obesity-resistant
             A/J mice. After 4 months, the feed efficiency ([FE] weight
             gained divided by calories consumed) did not differ across
             diets in A/J mice, but B/6J mice showed a significantly
             increased FE for fat. That is, B/6J mice gained more weight
             on high-fat diets without consuming more calories than A/J
             mice. The increase in FE was related to adipocyte
             hyperplasia in B/6J mice on high-fat diets. Fat-induced
             obesity in B/6J mice was unrelated to adrenal cortical
             activity. In the absence of fat, sucrose produced a
             decreased in FE in both strains. Animals fed a low-fat,
             high-sucrose (LH) diet were actually leaner than animals fed
             a high-complex-carbohydrate diet. Fat was also found to be
             the critical stimulus for hyperglycemia and hyperinsulinemia
             in B/6J mice. In the absence of fat, sucrose had no effect
             on plasma glucose or insulin. These data clearly show that
             across these two strains of mice, genetic differences in the
             metabolic response to fat are more important in the
             development of obesity and diabetes than the increased
             caloric content of a high-fat diet.},
   Doi = {10.1016/0026-0495(95)90123-x},
   Key = {fds276354}
}

@article{fds305796,
   Author = {OPARA, RC and PETRO, A and BROWN, S and FEINGLOS, MN and SURWIT,
             RS},
   Title = {EFFECT OF VITAMIN-E SUPPLEMENTATION ON DIET-INDUCED
             DIABETES},
   Journal = {Diabetes},
   Volume = {44},
   Pages = {A70-A70},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1995},
   Month = {May},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1995RA79600262&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305796}
}

@article{fds305801,
   Author = {OPARA, EC and PETRO, A and FEINGLOS, MN and SURWIT,
             RS},
   Title = {PREVENTIVE AND THERAPEUTIC EFFECTS OF L-GLUTAMINE ON
             DIET-INDUCED DIABETES},
   Journal = {Diabetes},
   Volume = {44},
   Pages = {A8-A8},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1995},
   Month = {May},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1995RA79600023&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305801}
}

@article{fds305803,
   Author = {OPARA, EC and PETRO, A and TEVRIZIAN, A and FEINGLOS, MN and SURWIT,
             RS},
   Title = {EFFECTS OF DIETARY-FAT REDUCTION AND L-GLUTAMINE
             SUPPLEMENTATION ON WEIGHT-GAIN},
   Journal = {Gastroenterology},
   Volume = {108},
   Number = {4},
   Pages = {A743-A743},
   Publisher = {W B SAUNDERS CO},
   Year = {1995},
   Month = {April},
   ISSN = {0016-5085},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1995QT86302963&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305803}
}

@article{fds141562,
   Title = {Wencel HC, Smothers C, Opara E, Kuhn C, Feinglos M, Surwit
             RS: Impaired second phase insulin response of diabetes-prone
             C57BL/6J mouse islets. Physiology and Behavior 57:
             1215-1220, 1995.},
   Year = {1995},
   Key = {fds141562}
}

@article{fds141563,
   Title = {Edens JL, Surwit RS: In support of behavioral treatment for
             day wetting in children. Urology 45: 904-907,
             1995.},
   Year = {1995},
   Key = {fds141563}
}

@article{fds141603,
   Title = {Surwit RS, Feinglos MN, Rodin J, Sutherland A, Petro AE,
             Opara EC, Kuhn M: Rebuffe-Scrive. Differential effects of
             fat and sucrose on the development of obesity and diabetes
             in C57BL/6J and A/J mice. Metabolism 44: 645-651,
             1995.},
   Year = {1995},
   Key = {fds141603}
}

@article{fds141611,
   Title = {Surwit RS, Feinglos MN, Rodin J, Sutherland A, Petro AE,
             Opara EC, Kuhn C, Rebuffe-Scrive M: Differential effects of
             fat and sucrose on the development of obesity and diabetes
             in C57BL/6J and A/J mice. Metabolism 44: 645-651,
             1995.},
   Year = {1995},
   Key = {fds141611}
}

@article{fds141612,
   Title = {Gettys WT, Ramkumar V, Cochrane C, Surwit R, Taylor IL:
             Tissue specific alterations in G-protein expression in
             genetic vs diet-induced models of NIDDM in the mouse.
             Metabolism 44: 771-778, 1995.},
   Year = {1995},
   Key = {fds141612}
}

@article{fds141613,
   Title = {Lee SK, Opara EC, Surwit RS, Feinglos MN, Akwari OE:
             Defective glucose-stimulated insulin release from perifused
             islets of C57BL/6J mice. Pancreas 11: 206-211,
             1995.},
   Year = {1995},
   Key = {fds141613}
}

@article{fds276384,
   Author = {Kuhn, CM and Surwit, RS and Feinglos, MN},
   Title = {Glipizide stimulates sympathetic outflow in diabetes-prone
             mice.},
   Journal = {Life Sciences},
   Volume = {56},
   Number = {9},
   Pages = {661-666},
   Year = {1995},
   ISSN = {0024-3205},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7869847},
   Keywords = {Animals • Diabetes Mellitus • Disease
             Susceptibility • Glipizide • Liver •
             Methyltyrosines • Mice • Mice, Inbred A •
             Mice, Inbred C57BL • Myocardium • Norepinephrine
             • Pancreas • drug effects • etiology* •
             metabolism • metabolism* • pharmacology •
             pharmacology*},
   Abstract = {The purpose of the present study was to determine if the
             oral hypoglycemic agent glipizide influenced sympathetic
             outflow in diabetes-prone mice. C57BL/6 (diabetes-prone) and
             diabetes-resistant (A/J) were treated with saline or
             glipizide, and sympathetic outflow determined by the fall in
             organ norepinephrine content after synthesis inhibition with
             alpha-methyl-para-tyrosine. Sympathetic outflow to the liver
             and pancreas were slower in Bl/6 mice than in control A/J.
             Glipizide increased sympathetic outflow to the pancreas in
             both strains of mice, but did not influence outflow to other
             organs significantly. The results of this study suggest that
             glipizide can influence central glucoregulatory mechanisms
             after peripheral administration.},
   Doi = {10.1016/0024-3205(94)00499-i},
   Key = {fds276384}
}

@article{fds276363,
   Author = {Esposito-Del Puente and A and Lillioja, S and Bogardus, C and McCubbin,
             JA and Feinglos, MN and Kuhn, CM and Surwit, RS},
   Title = {Glycemic response to stress is altered in euglycemic Pima
             Indians.},
   Journal = {Int J Obes Relat Metab Disord},
   Volume = {18},
   Number = {11},
   Pages = {766-770},
   Year = {1994},
   Month = {November},
   ISSN = {0307-0565},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7866478},
   Keywords = {Adolescent • Adult • Blood Glucose •
             Catecholamines • Diabetes Mellitus, Type 2 •
             European Continental Ancestry Group • Female •
             Glucagon • Glucose Tolerance Test • Humans •
             Hydrocortisone • Indians, North American • Insulin
             • Insulin Resistance • Male • Mathematics
             • Obesity • Prevalence • Radioimmunoassay
             • Risk Factors • Software • Stress,
             Psychological • analysis* • blood • blood*
             • complications • epidemiology • etiology
             • metabolism • physiopathology •
             psychology*},
   Abstract = {The aim of this work was to study the effects of a
             computer-driven mental arithmetic task on blood glucose in a
             group of four male and four female euglycemic Caucasians and
             a group of seven male and six female euglycemic Pima
             Indians. Approximately 60% of euglycemic Pima Indian Native
             Americans eventually develop type 2 diabetes, while only 5%
             of Caucasians develop the disease. All subjects had normal
             glucose tolerance. Subjects were given a standard breakfast;
             2 h later, they were given a computerized mental arithmetic
             stress test for 10 min. Before, during and after the test,
             several variables were analyzed, including serum
             concentrations of glucose, insulin, glucagon and plasma
             cortisol and catecholamines. Heart rate, systolic and
             diastolic blood pressure and all the stress hormones
             increased during stress and decreased during recovery in all
             subjects. Blood glucose consistently declined one hour after
             the meal in all subjects. However, while it continued to
             decline following stress in seven out of eight Caucasian
             subjects, it consistently increased during and following
             stress in 10 out of 13 Pima Indians. Fasting serum glucose
             in Pima Indians and Caucasians was respectively 5.07 + 0.08
             mM and 5.04 + 0.09 mM. Two-hour post-prandial values were
             5.63 + 0.22 mM and 5.48 + 0.19 mM respectively, whereas
             post-stress values were 6.15 + 0.19 mM for Pima Indians and
             5.22 + 0.20 mM for Caucasians. Both serum glucose means
             following stress (t = 3.1, P < 0.005) and the direction of
             change in serum glucose in response to mental arithmetic
             (chi 2 = 8.2, P < 0.01) clearly differentiated Pimas from
             Caucasians.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Key = {fds276363}
}

@article{fds276315,
   Author = {Robson, WL and Leung, AK and Mathers, MS},
   Title = {Kegel exercises and squatting behavior.},
   Journal = {The Journal of Pediatrics},
   Volume = {125},
   Number = {1},
   Pages = {169-170},
   Year = {1994},
   Month = {July},
   url = {http://dx.doi.org/10.1016/s0022-3476(94)70154-7},
   Doi = {10.1016/s0022-3476(94)70154-7},
   Key = {fds276315}
}

@article{fds276391,
   Author = {Seldin, MF and Mott, D and Bhat, D and Petro, A and Kuhn, CM and Kingsmore,
             SF and Bogardus, C and Opara, E and Feinglos, MN and Surwit,
             RS},
   Title = {Glycogen synthase: a putative locus for diet-induced
             hyperglycemia.},
   Journal = {The Journal of Clinical Investigation},
   Volume = {94},
   Number = {1},
   Pages = {269-276},
   Year = {1994},
   Month = {July},
   ISSN = {0021-9738},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8040269},
   Keywords = {Animals • Base Sequence • Blood Glucose •
             Chromosome Mapping* • Diabetes Mellitus, Type 2 •
             Glycogen Synthase • Insulin • Male • Mice
             • Mice, Inbred C3H • Mice, Inbred C57BL •
             Molecular Sequence Data • analysis • blood •
             genetics*},
   Abstract = {Inbred mouse strains fed a diabetogenic diet have different
             propensities to develop features analogous to type 2
             diabetes mellitus. To define chromosomal locations that
             control these characteristics, recombinant inbred strains
             from diabetes-prone C57BL/6J (B/6J) and diabetes-resistant
             A/J strains were studied. Insulin levels and hyperglycemia
             correlated with two different regions of mouse chromosome 7
             (two point LOD scores > 3.0). For insulin levels, 15 of 16
             recombinant inbred strains were concordant with a region
             that contains the tubby mutation that results in
             hyperinsulinemia. For hyperglycemia, 19 of 23 strains were
             concordant with the D7Mit25 marker and 20 of 23 strains with
             the Gpi-1 locus on proximal mouse chromosome 7. Using more
             stringent criteria for hyperglycemia, 10 of 11 strains
             characterized as A/J or B/6J like were concordant with
             D7Mit25. This putative susceptibility locus is consistent
             with that of the glycogen synthase gene (Gys) recently
             suggested as a candidate locus by analyses of type 2
             diabetes patients. Fractional glycogen synthase activity in
             isolated muscle was significantly lower in normal B/6J
             diabetic-prone mice compared with normal diabetic-resistant
             A/J mice, a finding similar to that reported in relatives of
             human patients with type 2 diabetes. These data, taken
             together, raise the possibility that defects in the Gys gene
             may in part be responsible for the propensity to develop
             type 2 diabetes.},
   Doi = {10.1172/JCI117317},
   Key = {fds276391}
}

@article{fds305777,
   Author = {SCHNEIDER, MS and KING, LR and SURWIT, RS},
   Title = {KEGEL EXERCISES AND SQUATTING BEHAVIOR -
             REPLY},
   Journal = {The Journal of Pediatrics},
   Volume = {125},
   Number = {1},
   Pages = {170-170},
   Publisher = {Mosby/Elsevier},
   Year = {1994},
   Month = {July},
   ISSN = {0022-3476},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1994NW31700037&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305777}
}

@article{fds276405,
   Author = {Livingston, EG and Feinglos, MN and Kuhn, CM and Secor, C and Surwit,
             RS},
   Title = {Hyperinsulinemia in the pregnant C57BL/6J
             mouse.},
   Journal = {Hormone and Metabolic Research},
   Volume = {26},
   Number = {6},
   Pages = {307-308},
   Year = {1994},
   Month = {June},
   ISSN = {0018-5043},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7927197},
   Keywords = {Animals • Disease Models, Animal* • Female •
             Insulin • Mice • Mice, Inbred C57BL •
             Pregnancy • Pregnancy in Diabetics •
             blood*},
   Doi = {10.1055/s-2007-1001690},
   Key = {fds276405}
}

@article{fds276418,
   Author = {Schneider, MS and King, LR and Surwit, RS},
   Title = {Kegel exercises and childhood incontinence: a new role for
             an old treatment.},
   Journal = {The Journal of Pediatrics},
   Volume = {124},
   Number = {1},
   Pages = {91-92},
   Year = {1994},
   Month = {January},
   ISSN = {0022-3476},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8283381},
   Keywords = {Adolescent • Child • Child, Preschool •
             Exercise Therapy* • Female • Humans • Male
             • Muscle, Smooth • Treatment Outcome •
             Urinary Incontinence • physiopathology •
             therapy*},
   Abstract = {Kegel exercises were used to treat urinary incontinence in
             79 children. An average of less than 2 hours of professional
             time was required. Incontinence was eliminated in 60% of the
             patients; children who had both day and night wetting tended
             to show simultaneous improvements in both problems. Research
             is needed to test the hypothesis that Kegel exercises
             eliminate involuntary contractions of the detrusor
             muscle.},
   Doi = {10.1016/s0022-3476(94)70259-4},
   Key = {fds276418}
}

@article{fds330733,
   Author = {Schneider, MS and King, LR and Surwit, RS},
   Title = {Reply to: Kegel exercises and squatting behavior},
   Journal = {The Journal of Pediatrics},
   Volume = {125},
   Number = {1},
   Pages = {169-170},
   Publisher = {Elsevier BV},
   Year = {1994},
   Month = {January},
   url = {http://dx.doi.org/10.1016/S0022-3476(94)70155-5},
   Doi = {10.1016/S0022-3476(94)70155-5},
   Key = {fds330733}
}

@article{fds141610,
   Title = {Schneider MS, King LR, Surwit RS: Kegel exercises and
             childhood incontinence: A new role for an old treatment.
             Journal of Pediatrics 124: 91-92, 1994.},
   Year = {1994},
   Key = {fds141610}
}

@article{fds276314,
   Author = {Surwit, RS},
   Title = {Of mice and men: Behavioral medicine in the study of type II
             diabetes},
   Journal = {Annals of Behavioral Medicine},
   Volume = {15},
   Number = {4},
   Pages = {227-235},
   Year = {1993},
   Month = {December},
   Abstract = {The development of a research program in behavioral medicine
             is reviewed from an historical perspective. Initial studies
             dealing with the effects of stress management on diabetes
             control are summarized. Questions raised by these studies
             led to a switch from human to animal studies. Results from
             these animal studies suggested that glucose responses to
             stress are characteristic of individuals predisposed to
             developing Type II diabetes. This hypothesis was then tested
             in humans. These studies led to the hypothesis that, while
             stress responsivity may be a marker for the development of
             diabetes, dietary effects on the sympathetic nervous system
             may be responsible for eventual appearance of the disease.
             Additionally, the development of a new animal model of Type
             II diabetes allowed new insights into the relationship of
             obesity and insulin resistance with the development of the
             disease itself. The evolution of this research program from
             one focused on behavioral variables to one with a more basic
             biological orientation is emphasized.},
   Key = {fds276314}
}

@article{fds276327,
   Author = {Rebuffé-Scrive, M and Surwit, R and Feinglos, M and Kuhn, C and Rodin,
             J},
   Title = {Regional fat distribution and metabolism in a new mouse
             model (C57BL/6J) of non-insulin-dependent diabetes
             mellitus.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {42},
   Number = {11},
   Pages = {1405-1409},
   Year = {1993},
   Month = {November},
   ISSN = {0026-0495},
   url = {http://dx.doi.org/10.1016/0026-0495(93)90190-y},
   Abstract = {It has been suggested that a genetic predisposition and an
             increased total fat mass, particularly a specific increase
             in visceral fat, contribute to the metabolic aberrations
             associated with human non-insulin-dependent diabetes
             mellitus (NIDDM). In this study, we investigated the
             interactions between genetic and dietary components on fat
             distribution and metabolism in two mouse strains, one
             genetically predisposed to NIDDM (BL/6) and one not (A/J),
             fed either a chow diet or a high-fat, high-simple
             carbohydrate (HFHSC) diet for 5 months. As expected, both
             strains of mice fed a HFHSC diet were heavier, had more fat
             in both the subcutaneous (inguinal [ING] and visceral
             (mesenteric [MES]) regions, and had larger fat cells and
             higher lipoprotein lipase (LPL) activities. The results of
             interactions between strain and diet showed important
             differences in fat distribution and metabolism between
             strains. In comparison with A/J mice, BL/6 mice fed a HFHSC
             diet developed hyperglycemia, hyperinsulinemia, and
             hypercholesterolemia, were heavier, had more overall fat,
             and particularly increased their MES adipose tissue. This
             increase in visceral fat mass was due to an increase in fat
             cell number. In contrast, BL/6 mice fed a chow diet had less
             overall fat, a smaller MES fat pad with smaller adipocytes,
             and lower LPL activity than A/J controls. Significant
             differences between BL/6 and A/J mice fed either a HFHSC or
             a chow diet were not observed in ING adipose tissue. These
             data suggest that in BL/6 mice, changes in the metabolic
             characteristics of visceral fat seem to be a specific
             characteristic associated with the genetic predisposition
             for NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Doi = {10.1016/0026-0495(93)90190-y},
   Key = {fds276327}
}

@article{fds276420,
   Author = {Lane, JD and McCaskill, CC and Ross, SL and Feinglos, MN and Surwit,
             RS},
   Title = {Relaxation training for NIDDM. Predicting who may
             benefit.},
   Journal = {Diabetes Care},
   Volume = {16},
   Number = {8},
   Pages = {1087-1094},
   Year = {1993},
   Month = {August},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8375238},
   Keywords = {Analysis of Variance • Anxiety • Biofeedback
             (Psychology) • Blood Glucose • Blood Pressure
             • Diabetes Mellitus, Type 2 • Epinephrine •
             Female • Follow-Up Studies • Glucose Tolerance
             Test • Hemoglobin A, Glycosylated • Humans •
             Internal-External Control • Male • Relaxation
             Techniques* • analysis • blood • metabolism*
             • physiopathology • psychology* •
             therapy},
   Abstract = {OBJECTIVE: To examine the benefits of relaxation training
             for patients with NIDDM and to investigate individual
             differences that could predict a positive response to
             relaxation training. RESEARCH DESIGN AND METHODS:
             Thirty-eight subjects with NIDDM were treated with intensive
             conventional diabetes therapy after an initial metabolic
             evaluation and psychological and pharmacological testing.
             Half were assigned to also receive biofeedback-assisted
             relaxation training. Treatment effects on GHb levels and
             glucose tolerance were evaluated after 8 wk. RESULTS:
             Subjects demonstrated significant improvements in GHb level,
             but not in glucose tolerance, after 8 wk of intensive
             conventional treatment. These improvements persisted
             throughout the follow-up period. However, the group provided
             with relaxation training did not experience greater
             improvements on either measure than the group given
             conventional diabetes treatment only. Within the group that
             received relaxation training, correlations occurred between
             the improvements in glucose tolerance after treatment and
             individual differences in trait anxiety and in the effect of
             alprazolam on glucose tolerance. Differences in the effects
             of EPI on glucose tolerance and personality measures of
             neuroticism and perceived locus of control also appeared to
             be related to improvements in glucose tolerance after
             training. CONCLUSIONS: Relaxation training did not confer
             added benefit over and above that provided by conventional
             diabetes treatment for patients with NIDDM. Additional
             research is needed to determine whether the administration
             of relaxation training to selected patients, especially
             those who are most responsive to stress, would provide
             benefits for glucose control that are not achieved by
             conventional treatment.},
   Doi = {10.2337/diacare.16.8.1087},
   Key = {fds276420}
}

@article{fds305784,
   Author = {SCHNEIDER, MS and SURWIT, RS and MCCASKILL, C},
   Title = {CEPHALIC PHASE INSULIN RESPONSES ARE MEDIATED BY CHANGES IN
             GLUCOSE},
   Journal = {Diabetes},
   Volume = {42},
   Pages = {A253-A253},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1993},
   Month = {May},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1993KZ62600803&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305784}
}

@article{fds276326,
   Author = {Mills, E and Kuhn, CM and Feinglos, MN and Surwit,
             R},
   Title = {Hypertension in CB57BL/6J mouse model of
             non-insulin-dependent diabetes mellitus.},
   Journal = {The American Journal of Physiology},
   Volume = {264},
   Number = {1 Pt 2},
   Pages = {R73-R78},
   Year = {1993},
   Month = {January},
   url = {http://dx.doi.org/10.1152/ajpregu.1993.264.1.R73},
   Abstract = {The C57BL/6J (BL/6) mouse develops non-insulin-dependent
             diabetes mellitus (NIDDM) when fed a high fat-high simple
             carbohydrate (HFHSC) diet, whereas A/J mice do not. The
             purpose of the study was to determine whether hypertension
             occurred with NIDDM and whether it was sustained by
             sympathetic nervous system (SNS) hyperactivity. After 3 mo
             on an HFHSC diet with a low Na content (0.06%), awake,
             tail-cuff systolic blood pressure (BP) increased 20% above
             the control diet in BL/6 (138 +/- 3 vs. 115 +/- 4) but not
             in A/J (115 +/- 6 vs. 113 +/- 2 mmHg) mice. On a normal Na
             (0.4%)-HFHSC diet, BL/6 mice had a higher BP than on 0.06%
             Na (149 +/- 3 at 3 mo, 162 +/- 6 at 4.5 mo). After 1 mo on
             the 0.06% Na-HFHSC diet, direct BP of anesthetized BL/6 mice
             was 18% higher than control. The hypotensive response to
             interruption of SNS activity by ganglionic blockade
             (chlorisondamine) increased in the BL/6 mice (50%), whereas
             the heart rate response increased in both strains (20-30%).
             Analysis of variance (ANOVA) on glucose detected significant
             effects of strain and diet and a strain x diet interaction
             (P = 0.0007). At 1 or 3 mo, HFHSC-fed BL/6 mice were
             hyperglycemic (> 11 mM) compared with diet or strain
             controls. The ANOVA on insulin detected strain and diet
             effects but not a strain x diet interaction (P = 0.3). HFHSC
             increased insulin above the control of 140-160 pM in A/J and
             BL/6 strain (20-70% at 1 mo, 400% at 3 mo).(ABSTRACT
             TRUNCATED AT 250 WORDS)},
   Doi = {10.1152/ajpregu.1993.264.1.R73},
   Key = {fds276326}
}

@article{fds141560,
   Title = {Mills E, Kuhn CM, Feinglos MN, Surwit RS: Hypertension in
             the C57BL/6J mouse model of non-insulin dependent diabetes
             mellitus. American Journal of Physiology 264 (33): R73-R78,
             1993.},
   Year = {1993},
   Key = {fds141560}
}

@article{fds141561,
   Title = {Rebuffe-Scrive M, Surwit R, Feinglos M, Kuhn C, Rodin J:
             Regional fat distribution and metabolism in new animal model
             (C57BL/6J) of NIDDM. Metabolism 42: 1405-1409,
             1993.},
   Year = {1993},
   Key = {fds141561}
}

@article{fds141607,
   Title = {Lane JD, McCaskill CC, Ross SL, Feinglos MN, Surwit RS:
             Relaxation training for non-insulin dependent diabetes:
             Predicting who will benefit. Diabetes Care 16: 1087-1094,
             1993.},
   Year = {1993},
   Key = {fds141607}
}

@article{fds141608,
   Title = {Surwit RS, Schneider MS: The role of stress in the etiology
             and treatment of diabetes mellitus. Psychosomatic Medicine
             55: 380-393, 1993.},
   Year = {1993},
   Key = {fds141608}
}

@article{fds141609,
   Title = {Surwit RS: Of mice and men: Behavioral medicine in the study
             of type II diabetes. Annals of Behavioral Medicine 15:
             227-235, 1993.},
   Year = {1993},
   Key = {fds141609}
}

@article{fds276429,
   Author = {Surwit, RS and Schneider, MS},
   Title = {Role of stress in the etiology and treatment of diabetes
             mellitus.},
   Journal = {Psychosomatic Medicine},
   Volume = {55},
   Number = {4},
   Pages = {380-393},
   Year = {1993},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8105502},
   Keywords = {Animals • Anti-Anxiety Agents • Blood Glucose
             • Catecholamines • Cats • Combined Modality
             Therapy • Diabetes Mellitus, Type 1 • Diabetes
             Mellitus, Type 2 • Female • Humans •
             Hyperglycemia • Hypoglycemia • Male • Mice
             • Norepinephrine • Rats • Relaxation
             Techniques • Stress, Psychological • Sympathetic
             Nervous System • complications* • etiology* •
             metabolism • therapeutic use •
             therapy},
   Abstract = {Stress has long been suspected as having major effects on
             metabolic activity. The effects of stress on glucose
             metabolism are mediated by a variety of "counter-regulatory"
             hormones that are released in response to stress and that
             result in elevated blood glucose levels and decreased
             insulin action. This energy mobilizing effect is of adaptive
             importance in a healthy organism. However, in diabetes,
             because of a relative or absolute lack of insulin,
             stress-induced increases in blood glucose cannot be
             adequately metabolized. Thus, stress is a potential
             contributor to chronic hyperglycemia in diabetes, although
             its exact role is unclear. Although there is some suggestion
             from retrospective human studies that stress can precipitate
             type I diabetes, animal studies are contradictory with
             different stressors either having facilitatory or inhibitory
             effects upon the development of the disease. Human
             investigations in patients with established diabetes are
             equally confusing with some showing that stress can
             stimulate hyperglycemia, hypoglycemia or have no effect at
             all on glycemic status. There is more consistent evidence
             supporting the role of stress in animal models of type II
             diabetes. However, human studies on the role of stress on
             the course of established type II diabetes are few.
             Intervention studies suggest that behavioral or
             pharmacologic intervention to manage stress may contribute
             significantly to diabetes treatment, but more long-term
             research is needed. It is concluded that further research is
             needed to establish the importance of behavioral factors in
             the etiology and management of diabetes, and several areas
             of methodologic improvement are suggested.},
   Doi = {10.1097/00006842-199307000-00005},
   Key = {fds276429}
}

@article{fds276432,
   Author = {Surwit, RS and Schneider, MS and Feinglos, MN},
   Title = {Stress and diabetes mellitus.},
   Journal = {Diabetes Care},
   Volume = {15},
   Number = {10},
   Pages = {1413-1422},
   Year = {1992},
   Month = {October},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1425110},
   Keywords = {Animals • Blood Glucose • Diabetes Mellitus •
             Diabetes Mellitus, Type 1 • Diabetes Mellitus, Type 2
             • Humans • Mice • Mice, Obese • Stress
             • Stress, Psychological • metabolism •
             physiopathology • physiopathology* • psychology
             • psychology*},
   Abstract = {Stress is a potential contributor to chronic hyperglycemia
             in diabetes. Stress has long been shown to have major
             effects on metabolic activity. Energy mobilization is a
             primary result of the fight or flight response. Stress
             stimulates the release of various hormones, which can result
             in elevated blood glucose levels. Although this is of
             adaptive importance in a healthy organism, in diabetes, as a
             result of the relative or absolute lack of insulin,
             stress-induced increases in glucose cannot be metabolized
             properly. Furthermore, regulation of these stress hormones
             may be abnormal in diabetes. However, evidence
             characterizing the effects of stress in type I diabetes is
             contradictory. Although some retrospective human studies
             have suggested that stress can precipitate type I diabetes,
             animal studies have shown that stressors of various kinds
             can precipitate--or prevent--various experimental models of
             the disease. Human studies have shown that stress can
             stimulate hyperglycemia, hypoglycemia, or have no affect at
             all on glycemic status in established diabetes. Much of this
             confusion may be attributable to the presence of autonomic
             neuropathy, common in type I diabetes. In contrast, more
             consistent evidence supports the role of stress in type II
             diabetes. Although human studies on the role of stress in
             the onset and course of type II diabetes are few, a large
             body of animal study supports the notion that stress
             reliably produces hyperglycemia in this form of the disease.
             Furthermore, there is mounting evidence of autonomic
             contributions to the pathophysiology of this condition in
             both animals and humans.},
   Doi = {10.2337/diacare.15.10.1413},
   Key = {fds276432}
}

@article{fds276430,
   Author = {Feinglos, MN and Surwit, RS and McCaskill, CC and Ross,
             SL},
   Title = {Plasma levels of beta-endorphin and adrenocorticotropic
             hormone in IDDM and NIDDM.},
   Journal = {Diabetes Care},
   Volume = {15},
   Number = {4},
   Pages = {590-591},
   Year = {1992},
   Month = {April},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1323455},
   Keywords = {Adrenocorticotropic Hormone • Adult • Analysis of
             Variance • Blood Glucose • Diabetes Mellitus, Type
             1 • Diabetes Mellitus, Type 2 • Female •
             Humans • Hydrocortisone • Male • analysis
             • beta-Endorphin • blood •
             blood*},
   Doi = {10.2337/diacare.15.4.590},
   Key = {fds276430}
}

@article{fds276399,
   Author = {Surwit, RS and Lane, JD},
   Title = {Physical activity and non-insulin dependent diabetes
             mellitus.},
   Journal = {The New England Journal of Medicine},
   Volume = {325},
   Number = {26},
   Pages = {1887},
   Year = {1991},
   Month = {December},
   ISSN = {0028-4793},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1797001},
   Keywords = {Diabetes Mellitus, Type 2 • Exercise* • Humans
             • prevention & control*},
   Doi = {10.1056/NEJM199112263252616},
   Key = {fds276399}
}

@article{fds305790,
   Author = {MILLS, E and KUHN, CM and FEINGLOSS, MN and SURWIT,
             RS},
   Title = {HYPERTENSION IN RELATION TO DIET INDUCED DIABETES (NIDDM) IN
             C57BL/6J MICE},
   Journal = {Faseb Journal},
   Volume = {5},
   Number = {6},
   Pages = {A1482-A1482},
   Publisher = {FEDERATION AMER SOC EXP BIOL},
   Year = {1991},
   Month = {March},
   ISSN = {0892-6638},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1991FE55700142&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305790}
}

@article{fds276365,
   Author = {Surwit, RS and Seldin, MF and Kuhn, CM and Cochrane, C and Feinglos,
             MN},
   Title = {Control of expression of insulin resistance and
             hyperglycemia by different genetic factors in diabetic
             C57BL/6J mice.},
   Journal = {Diabetes},
   Volume = {40},
   Number = {1},
   Pages = {82-87},
   Year = {1991},
   Month = {January},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2015977},
   Keywords = {Animals • Blood Glucose • Crosses, Genetic •
             Diabetes Mellitus, Experimental • Female •
             Hyperglycemia • Insulin • Insulin Resistance
             • Male • Mice • Mice, Inbred C57BL •
             Mice, Inbred Strains • Recombination, Genetic •
             analysis • blood • genetics* •
             physiopathology},
   Abstract = {The inheritance of the tendency to develop diet-induced
             non-insulin-dependent (type II) diabetes was analyzed in
             crosses between diabetes-prone C57BL/6J (BL/6) mice and
             diabetes-resistant A/J mice. The effects of a diabetogenic
             diet on blood glucose and insulin levels, insulin
             sensitivity, and weight were evaluated in F1 and both (BL/6
             X A/J) F1 X BL/6 and (BL/6 X A/J) F1 X A/J backcross mice.
             These results suggest that diet-induced hyperglycemia is
             largely determined by a recessive gene and diet-induced
             insulin resistance by a dominant gene. Analyses of both
             backcrosses indicated that insulin sensitivity and blood
             glucose levels were unrelated, suggesting that they are
             controlled by different genetic factors. This conclusion was
             supported by data from nine recombinant inbred BXA strains
             in which no correlation was observed between these
             variables. Furthermore, insulin sensitivity and body weight
             correlated differently in the two backcross groups,
             suggesting that insulin resistance is not simply a function
             of obesity. The number of genes that predominantly influence
             diabetic traits was estimated by comparing the variance
             observed in (BL/6 X A/J) F1 X BL/6 backcross mice with that
             observed in parental mice. The data suggest that relatively
             few genes predominantly affect the diabetic phenotype in
             this murine model.},
   Doi = {10.2337/diab.40.1.82},
   Key = {fds276365}
}

@article{fds276356,
   Author = {McCubbin, JA and Surwit, RS and Williams, RB and Nemeroff, CB and McNeilly, M},
   Title = {Altered pituitary hormone response to naloxone in
             hypertension development.},
   Journal = {Hypertension},
   Volume = {14},
   Number = {6},
   Pages = {636-644},
   Year = {1989},
   Month = {December},
   ISSN = {0194-911X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2555303},
   Keywords = {Adolescent • Adrenocorticotropic Hormone • Adult
             • Blood Pressure • Epinephrine • Humans
             • Hydrocortisone • Hypertension • Male •
             Naloxone • Stress, Psychological • beta-Endorphin
             • blood • blood* • drug effects* •
             pharmacology*},
   Abstract = {Endogenous opioid regulation of blood pressure is altered
             during stress in young adults at risk for hypertension. We
             studied the effects of the opioid antagonist naloxone on the
             secretion of corticotropin and beta-endorphin during
             psychological stress in young adults with mildly elevated
             casual arterial pressures. Naloxone-induced secretion of
             both corticotropin and beta-endorphin was significantly
             diminished in persons at enhanced risk for hypertension
             compared with the low blood pressure control group. Results
             suggest that opioidergic inhibition of anterior pituitary
             function is altered in hypertension development.},
   Doi = {10.1161/01.hyp.14.6.636},
   Key = {fds276356}
}

@article{fds276434,
   Author = {Fukudo, S and Virnelli, S and Kuhn, CM and Cochrane, C and Feinglos, MN and Surwit, RS},
   Title = {Muscarinic stimulation and antagonism and glucoregulation in
             nondiabetic and obese hyperglycemic mice.},
   Journal = {Diabetes},
   Volume = {38},
   Number = {11},
   Pages = {1433-1438},
   Year = {1989},
   Month = {November},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2576006},
   Keywords = {Animals • Atropine • Bethanechol •
             Bethanechol Compounds • Blood Glucose •
             Dose-Response Relationship, Drug • Glucagon •
             Glucose • Homeostasis • Insulin • Liver
             • Mice • Mice, Obese • Propranolol •
             blood • blood* • metabolism • metabolism*
             • pharmacology • pharmacology* •
             physiology*},
   Abstract = {Plasma glucose and insulin responses to a muscarinic agonist
             (bethanechol chloride) and a muscarinic antagonist
             (atropine) were evaluated in obese C57BL/6J ob/ob mice and
             in lean C57BL/6J + /? mice. In lean +/? mice, plasma glucose
             decreased in response to 1 and 2 micrograms/g bethanechol
             chloride, whereas insulin increased significantly. In ob/ob
             mice, insulin increased remarkably in response to
             bethanechol administration (saline, 632 +/- 80 microU/ml; 2
             micrograms/g bethanechol chloride, 1794 +/- 97 microU/ml; n
             = 10), but surprisingly, plasma glucose also rose
             significantly (saline, 230 +/- 14 mg/dl; 2 micrograms/g
             bethanechol chloride, 363 +/- 18 mg/dl, n = 10). This
             exaggerated hyperglycemia in ob/ob mice was not associated
             with significant changes in plasma glucagon. Furthermore,
             administration of propranolol hydrochloride did not diminish
             bethanechol chloride-induced hyperglycemia in ob/ob mice.
             Administration of atropine (2.5, 5, and 10 mg/kg body wt)
             induced a significant decrease in plasma insulin without
             changes in plasma glucose in ob/ob mice, whereas neither
             plasma insulin nor plasma glucose changed in lean mice.
             Finally, conversion of [14C]alanine to glucose was increased
             in ob/ob mice after bethanechol chloride administration,
             indicating that muscarinic stimulation increases
             gluconeogenesis in an animal model of type II
             (non-insulin-dependent) diabetes.},
   Doi = {10.2337/diab.38.11.1433},
   Key = {fds276434}
}

@article{fds276428,
   Author = {Surwit, RS and McCubbin, JA and Kuhn, CM and Cochrane, C and Feinglos,
             MN},
   Title = {Differential glycemic effects of morphine in diabetic and
             normal mice.},
   Journal = {Metabolism: Clinical and Experimental},
   Volume = {38},
   Number = {3},
   Pages = {282-285},
   Year = {1989},
   Month = {March},
   ISSN = {0026-0495},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2645504},
   Keywords = {Animals • Blood Glucose • Diabetes Mellitus •
             Insulin • Mice • Mice, Inbred C57BL • Mice,
             Inbred Strains • Mice, Obese • Morphine •
             Obesity* • Stress • analysis* • blood •
             blood* • pharmacology*},
   Abstract = {C57BL/6J ob/ob mice, C57BL/6J+/? lean mice and A/J mice were
             given injections of 10 mg/kg of morphine or an equal volume
             of saline, and then blood was sampled by retroorbital sinus
             puncture. In addition, animals from each strain were exposed
             to a brief experimental stress ten minutes after the
             administration of morphine or saline. While morphine
             produced significant increases in serum glucose in albino
             mice, morphine lowered blood insulin in both C57BL/6J ob/ob
             and C57BL/6J+/? mice. Morphine significantly lowered blood
             insulin in A/J mice, but effects in C57BL/6J mice were not
             significant. In contrast, morphine attenuated blood glucose
             and insulin during stress in C57BL/6J ob/ob but did not
             significantly affect either glucose or insulin during stress
             in lean C57BL/6J or A/J mice. These results are interpreted
             in the light of other data suggesting that endogenous
             opiates modulate the effects of sympathetic nervous system
             activity in type II diabetes.},
   Doi = {10.1016/0026-0495(89)90089-9},
   Key = {fds276428}
}

@article{fds276377,
   Author = {McCubbin, JA and Surwit, RS and Kuhn, CM and Cochrane, C and Feinglos,
             MN},
   Title = {Naltrexone potentiates glycemic responses during stress and
             epinephrine challenge in genetically obese
             mice.},
   Journal = {Psychosomatic Medicine},
   Volume = {51},
   Number = {4},
   Pages = {441-448},
   Year = {1989},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2549557},
   Keywords = {Animals • Arousal • Blood Glucose • Diabetes
             Mellitus • Diabetes Mellitus, Experimental •
             Epinephrine • Mice • Mice, Inbred C57BL •
             Mice, Obese • Naltrexone • Obesity* •
             Receptors, Opioid • Stress, Psychological • blood*
             • complications* • drug effects* • genetics
             • metabolism* • pharmacology*},
   Abstract = {The genetically obese mouse (C57BL/6J ob/ob) is a commonly
             used animal model of non-insulin-dependent diabetes
             mellitus. These mice show exaggerated glycemic responses
             during behavioral stress and adrenergic stimulation, but the
             precise glucoregulatory mechanisms are not well
             characterized. The ob/ob mice have multiple endocrine
             abnormalities, including elevated pituitary and circulating
             beta-endorphin levels; and a relationship between
             hyperglycemia and altered opioid function has been
             suspected. We now report that opiate antagonism with
             naltrexone potentiates hyperglycemic responses during stress
             and epinephrine challenge in obese mice. This effect of
             opioid blockade suggests that endogenous opioids inhibit
             stress- and epinephrine-induced hyperglycemia in the
             genetically obese mouse.},
   Doi = {10.1097/00006842-198907000-00007},
   Key = {fds276377}
}

@article{fds276431,
   Author = {Surwit, RS and Kuhn, CM and Cochrane, C and McCubbin, JA and Feinglos,
             MN},
   Title = {Diet-induced type II diabetes in C57BL/6J
             mice.},
   Journal = {Diabetes},
   Volume = {37},
   Number = {9},
   Pages = {1163-1167},
   Publisher = {American Diabetes Association},
   Year = {1988},
   Month = {September},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3044882},
   Keywords = {Animals • Blood Glucose • Corticosterone •
             Diabetes Mellitus, Experimental • Diabetes Mellitus,
             Type 2 • Diet* • Epinephrine • Insulin •
             Insulin Resistance • Male • Mice • Mice,
             Inbred A • Mice, Inbred C57BL • Obesity •
             Species Specificity • Stress • blood •
             etiology • metabolism • pharmacology •
             physiopathology • physiopathology*},
   Abstract = {We investigated the effects of diet-induced obesity on
             glucose metabolism in two strains of mice, C57BL/6J and A/J.
             Twenty animals from each strain received ad libitum exposure
             to a high-fat high-simple-carbohydrate diet or standard
             Purina Rodent Chow for 6 mo. Exposure to the high-fat,
             high-simple-carbohydrate, low-fiber diet produced obesity in
             both A/J and C57BL/6J mice. Whereas obesity was associated
             with only moderate glucose intolerance and insulin
             resistance in A/J mice, obese C57BL/6J mice showed clear-cut
             diabetes with fasting blood glucose levels of greater than
             240 mg/dl and blood insulin levels of greater than 150
             microU/ml. C57BL/6J mice showed larger glycemic responses to
             stress and epinephrine in the lean state than AJ mice, and
             these responses were exaggerated by obesity. These data
             suggest that the C57BL/6J mouse carries a genetic
             predisposition to develop non-insulin-dependent (type II)
             diabetes. Furthermore, altered glycemic response to
             adrenergic stimulation may be a biologic marker for this
             genetic predisposition to develop type II
             diabetes.},
   Doi = {10.2337/diab.37.9.1163},
   Key = {fds276431}
}

@article{fds305769,
   Author = {MCCUBBIN, JA and SURWIT, RS and WILLIAMS, RB and STELZENMULLER,
             ME},
   Title = {RELIABILITY AND VALIDITY OF CASUAL BLOOD PRESSURES -
             RELATIONSHIP BETWEEN FIELD AND LABORATORY
             VALUES},
   Journal = {Psychophysiology},
   Volume = {25},
   Number = {4},
   Pages = {468-468},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1988},
   Month = {July},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1988P919200191&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305769}
}

@article{fds276370,
   Author = {Stabler, B and Lane, JD and Ross, SL and Morris, MA and Litton, J and Surwit, RS},
   Title = {Type A behavior pattern and chronic glycemic control in
             individuals with IDDM.},
   Journal = {Diabetes Care},
   Volume = {11},
   Number = {4},
   Pages = {361-362},
   Year = {1988},
   Month = {April},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3402294},
   Keywords = {Adolescent • Blood Glucose • Child • Diabetes
             Mellitus, Type 1 • Female • Humans • Male
             • Type A Personality* • blood • metabolism*
             • psychology*},
   Doi = {10.2337/diacare.11.4.361},
   Key = {fds276370}
}

@article{fds305789,
   Author = {STABLER, B and LANE, JD and ROSS, SL and MORRIS, MA and SURWIT,
             RS},
   Title = {PSYCHOLOGICAL CORRELATES OF CHRONIC BLOOD-GLUCOSE CONTROL IN
             DIABETIC CHILDREN AND ADOLESCENTS},
   Journal = {Psychosomatic Medicine},
   Volume = {50},
   Number = {2},
   Pages = {194-194},
   Publisher = {WILLIAMS & WILKINS},
   Year = {1988},
   Month = {March},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1988M721400014&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305789}
}

@article{fds276387,
   Author = {Surwit, RS and Feinglos, MN},
   Title = {Stress and autonomic nervous system in type II diabetes. A
             hypothesis.},
   Journal = {Diabetes Care},
   Volume = {11},
   Number = {1},
   Pages = {83-85},
   Year = {1988},
   Month = {January},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3276481},
   Keywords = {Animals • Blood Glucose • Diabetes Mellitus, Type
             2 • Humans • Hyperglycemia • Insulin •
             Mice • Stress • Sympathetic Nervous System •
             metabolism • physiopathology • physiopathology*
             • secretion},
   Doi = {10.2337/diacare.11.1.83},
   Key = {fds276387}
}

@article{fds276362,
   Author = {Morrell, EM and Surwit, RS and Kuhn, CM and Feinglos, MN and Cochrane,
             C},
   Title = {Classically conditioned enhancement of hyperinsulinemia in
             the ob/ob mouse.},
   Journal = {Psychosomatic Medicine},
   Volume = {50},
   Number = {6},
   Pages = {586-590},
   Year = {1988},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3070619},
   Keywords = {Animals • Arousal • Blood Glucose • Body
             Weight* • Conditioning, Classical • Insulin •
             Male • Mice • Mice, Inbred C57BL • Mice,
             Obese • Smell • blood* • metabolism* •
             physiology • physiology*},
   Abstract = {The obese (C57BL/6J ob/ob) mouse is a commonly used animal
             model of non-insulin-dependent diabetes mellitus. Recent
             experiments have shown that stress hyperglycemia can be
             classically conditioned in the obese but not in the lean
             mouse. In the present study, classical conditioning of
             insulin secretion was attempted in C57BL/6J obese and lean
             animals. For 21 days, obese and lean mice were exposed to a
             conditioned olfactory stimulus prior to and during eating.
             On the 22nd day, blood was sampled for all animals following
             presentation of the conditioned stimulus; testing was
             repeated 2 weeks later following an additional 4 days of
             conditioning. Results indicated an effect of conditioning,
             with significantly greater plasma insulin for trained than
             for untrained obese mice. That insulin secretion can be more
             easily conditioned in the obese mouse suggests that a
             cholinergic mechanism may be involved in the
             hyperinsulinemia characteristic of this animal.},
   Doi = {10.1097/00006842-198811000-00004},
   Key = {fds276362}
}

@article{fds276385,
   Author = {McCubbin, JA and Surwit, RS and Williams, RB},
   Title = {Opioid dysfunction and risk for hypertension: naloxone and
             blood pressure responses during different types of
             stress.},
   Journal = {Psychosomatic Medicine},
   Volume = {50},
   Number = {1},
   Pages = {8-14},
   Year = {1988},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2830632},
   Keywords = {Adolescent • Adult • Arousal • Autonomic
             Nervous System • Blood Pressure • Humans •
             Hypertension • Male • Naloxone • Neural
             Inhibition • Posture • Problem Solving •
             Receptors, Opioid • drug effects • drug effects*
             • pharmacology* • physiology • physiology*
             • physiopathology • physiopathology*},
   Abstract = {Opioidergic inhibition of sympathetic nervous system
             responses may be deficient in persons at risk for essential
             hypertension (McCubbin et al: Hypertension 7:808, 1985). The
             opiate antagonist naloxone increases blood pressure
             responses during psychological stress in young adults with
             low causal blood pressure, but has no pressor effect in
             subjects with high casual blood pressure. The purpose of the
             present study was to determine the role of altered
             baroreflex function in the abnormal pressor effect of
             naloxone in persons at risk for hypertension development. We
             tested this by comparison of the effects of naloxone on
             responses to psychological stress with responses to
             orthostatic stress in persons with high and low casual blood
             pressure. The results suggest that abnormal opioidergic
             control of systolic blood pressure responses to
             psychological stress is not likely a result of altered
             baroreflex function. Persons at risk for hypertension show
             evidence of an opioid peptide lesion that can probably be
             localized either at the adrenal medullae or at levels of
             central autonomic control that are parallel with or rostral
             to baroreflex circuits.},
   Doi = {10.1097/00006842-198801000-00002},
   Key = {fds276385}
}

@article{fds276398,
   Author = {Lane, JD and Stabler, B and Ross, SL and Morris, MA and Litton, JC and Surwit, RS},
   Title = {Psychological predictors of glucose control in patients with
             IDDM.},
   Journal = {Diabetes Care},
   Volume = {11},
   Number = {10},
   Pages = {798-800},
   Year = {1988},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3246201},
   Keywords = {Adolescent • Blood Glucose • Blood Glucose
             Self-Monitoring • Diabetes Mellitus, Type 1 •
             Female • Hemoglobin A, Glycosylated • Humans
             • Male • Patient Compliance • Personality
             Tests • Personality* • Prognosis • analysis
             • analysis* • blood • psychology*},
   Doi = {10.2337/diacare.11.10.798},
   Key = {fds276398}
}

@article{fds305802,
   Author = {Surwit, RS and Feinglos, MN},
   Title = {Relaxation Therapy: A Reply},
   Journal = {Diabetes Care},
   Volume = {10},
   Number = {6},
   Pages = {794-795},
   Publisher = {American Diabetes Association},
   Year = {1987},
   Month = {November},
   ISSN = {0149-5992},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1987L246800034&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Doi = {10.2337/diacare.10.6.794b},
   Key = {fds305802}
}

@article{fds305776,
   Author = {MCCUBBIN, JA and SURWIT, RS and WILLIAMS, RB and NEMEROFF,
             CB},
   Title = {ABNORMAL OPIOIDERGIC INHIBITION OF THE HYPOTHALAMIC-PITUITARY-ADRENOCORTICAL
             AXIS IN HUMANS AT RISK FOR HYPERTENSION},
   Journal = {Psychophysiology},
   Volume = {24},
   Number = {5},
   Pages = {600-600},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1987},
   Month = {September},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1987J727200127&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305776}
}

@article{fds276379,
   Author = {Hand, MS and Surwit, RS and Rodin, J and Van Order and P and Feinglos,
             MN},
   Title = {Failure of genetically selected miniature swine to model
             NIDDM.},
   Journal = {Diabetes},
   Volume = {36},
   Number = {3},
   Pages = {284-287},
   Year = {1987},
   Month = {March},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3542650},
   Keywords = {Animals • Blood Glucose • Diabetes Mellitus, Type
             2* • Diet • Disease Models, Animal* • Female
             • Glucose Tolerance Test • Insulin • Male
             • Swine • Swine, Miniature • analysis •
             blood • genetics* • metabolism},
   Abstract = {Ten young adult miniature swine from a line reported to be
             genetically selected for glucose intolerance and eight
             normal controls were obtained from Colorado State
             University. They were consecutively exposed to 4 mo of a
             high-fiber, low-fat standard swine diet; 4 mo of a
             high-sucrose, high-fat, low-fiber diabetogenic diet; and 4
             mo of excess diabetogenic diet for obesification. Results of
             oral glucose tolerance and intravenous insulin tolerance
             tests conducted at the end of each regimen were compared.
             Hyperglycemia was not observed in any animals after any
             manipulation. Insulin sensitivity was also not influenced by
             diet. We conclude that F7 low-K miniature swine from this
             colony fail to model human non-insulin-dependent
             diabetes.},
   Doi = {10.2337/diab.36.3.284},
   Key = {fds276379}
}

@article{fds276390,
   Author = {Kuhn, CM and Cochrane, C and Feinglos, MN and Surwit,
             RS},
   Title = {Exaggerated peripheral responses to catecholamines
             contributes to stress-induced hyperglycemia in the ob/ob
             mouse.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {26},
   Number = {3},
   Pages = {491-495},
   Year = {1987},
   Month = {March},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3554269},
   Keywords = {Adrenergic Fibers • Animals • Blood Glucose •
             Diabetes Mellitus • Dose-Response Relationship, Drug
             • Epinephrine • Fasting • Hyperglycemia
             • Insulin • Mice • Mice, Inbred C57BL •
             Mice, Obese • Obesity* • Phentolamine •
             Stress • blood • blood* • drug effects •
             metabolism • pharmacology* • physiology •
             physiopathology*},
   Abstract = {The present study investigated the contribution of altered
             sympathetic reactivity to the stress-induced hyperglycemia
             observed in the c57BL/6J (ob/ob) mouse, an animal model of
             type II diabetes. Blood glucose and insulin responses to
             sympathetic agonist and antagonist administration were
             evaluated in ob/ob mice and their nondiabetic, lean (ob/?)
             littermates. In addition, the ability of nutritional status
             to modify these responses was determined. These studies
             demonstrated that epinephrine administration to ob/ob mice
             caused an exaggerated increase in blood glucose and decrease
             in plasma insulin in ob/ob mice relative to lean
             littermates. The dose response curve for epinephrine-induced
             increases in blood glucose were shifted to the left, and the
             duration of the blood glucose and plasma insulin responses
             was longer. Differences between ob/ob mice and their
             nondiabetic littermates were greater when animals were
             tested in the fasted state. In addition, administration of
             the alpha adrenergic antagonist phentolamine caused a larger
             increase in plasma insulin in ob/ob mice than was observed
             in lean littermates. These results suggest that altered
             peripheral responses to sympathetic stimuli contribute to
             stress-induced hyperglycemia in ob/ob mice, and raise the
             possibility that altered sympathetic function is an
             etiologic factor in development of diabetes in these
             animals.},
   Doi = {10.1016/0091-3057(87)90154-7},
   Key = {fds276390}
}

@article{fds276313,
   Author = {McCubbin, JA and Surwit, RS and Mansbach, CM},
   Title = {Sensory discrimination training in the treatment of a case
             of chronic constipation},
   Journal = {Behavior Therapy},
   Volume = {18},
   Number = {3},
   Pages = {273-278},
   Publisher = {Elsevier BV},
   Year = {1987},
   Month = {January},
   ISSN = {0005-7894},
   url = {http://dx.doi.org/10.1016/S0005-7894(87)80021-7},
   Abstract = {A 31-year-old woman with a history of life-long constipation
             and laxative dependence was treated with discrimination
             training for rectal sensation. She had complained of absence
             of the urge to defecate, bloating with abdominal discomfort,
             and need for laxatives to relieve symptoms. Manometric
             examination with an anorectal balloon assembly revealed a
             normal threshold for sphincteric reflexes, but an abnormally
             elevated threshold for detection of rectal distention.
             Behavioral treatment consisted of a manometrically based
             sensory discrimination procedure designed to reduce the
             sensory threshold for rectal distention. Multiple training
             sessions with this procedure allowed recognition of
             progressively smaller rectal distention volumes.
             Accompanying these changes in rectal sensory threshold were
             concomitant increases in the frequency of bowel movements,
             decreases in the weekly use of laxatives, and decreases in
             subjective discomfort. Therapeutic effects were maintained
             at follow-up examination one year later. The results of this
             case study suggest that behavioral training to increase
             rectal sensation may be useful in treating constipation in
             patients who have abnormal rectal sensory thresholds. ©
             1987 Association for Advancement of Behavior Therapy. All
             rights reserved.},
   Doi = {10.1016/S0005-7894(87)80021-7},
   Key = {fds276313}
}

@article{fds305805,
   Author = {Surwit, RS and Feinglos, MN},
   Title = {Cognitive Functioning and Diabetes: A Reply},
   Journal = {Diabetes Care},
   Volume = {10},
   Number = {1},
   Pages = {136-137},
   Publisher = {American Diabetes Association},
   Year = {1987},
   Month = {January},
   ISSN = {0149-5992},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1987F969100027&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Doi = {10.2337/diacare.10.1.136},
   Key = {fds305805}
}

@article{fds276386,
   Author = {Stabler, B and Surwit, RS and Lane, JD and Morris, MA and Litton, J and Feinglos, MN},
   Title = {Type A behavior pattern and blood glucose control in
             diabetic children.},
   Journal = {Psychosomatic Medicine},
   Volume = {49},
   Number = {3},
   Pages = {313-316},
   Year = {1987},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3602301},
   Keywords = {Adolescent • Arousal • Blood Glucose • Child
             • Diabetes Mellitus, Type 1 • Female • Humans
             • Male • Type A Personality* • blood •
             metabolism* • physiology • psychology*},
   Abstract = {We studied the relationship between presence of Type A
             behavior pattern and glycemic response to stress in children
             with insulin dependent diabetes mellitus (IDDM). Twelve male
             (six Type A and six Type B) and nine female (four Type A and
             five Type B) insulin-dependent diabetic patients between the
             ages of 8 and 16 years received a standard meal and blood
             glucose values were assessed two hours later. All subjects
             then played a competitive videogame for 10 minutes following
             which blood glucose was assessed again. Preprandial and
             postprandial blood glucose values did not differ between the
             groups. However, only Type A subjects showed a hyperglycemic
             response to the videogame stress. Type A subjects also
             demonstrated significantly higher glycohemoglobin values. In
             order to assure that this effect was due to a differential
             response to stress and not simply a difference in metabolic
             response to a meal, a second study was conducted in which
             blood glucose values were assessed at one, two and three
             hours following a standard meal. No significant differences
             in postprandial blood glucose values were observed between
             Type A and Type B subjects. These data support previous
             research which has suggested that some but not all patients
             with IDDM show a hyperglycemic response to
             stress.},
   Doi = {10.1097/00006842-198705000-00010},
   Key = {fds276386}
}

@article{fds276427,
   Author = {Feinglos, MN and Hastedt, P and Surwit, RS},
   Title = {Effects of relaxation therapy on patients with type I
             diabetes mellitus.},
   Journal = {Diabetes Care},
   Volume = {10},
   Number = {1},
   Pages = {72-75},
   Year = {1987},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3552516},
   Keywords = {Adult • Biofeedback (Psychology)* • Blood Glucose
             • Diabetes Mellitus, Type 1 • Diabetes Mellitus,
             Type 2 • Electromyography • Epinephrine •
             Female • Humans • Hydrocortisone • Insulin
             • Male • Muscle Contraction* • Muscle
             Relaxation* • Norepinephrine • administration &
             dosage • blood • drug therapy • metabolism
             • therapeutic use • therapy •
             therapy*},
   Abstract = {We investigated the effect of treatment with
             biofeedback-associated progressive muscle relaxation on 10
             patients with poorly controlled type I diabetes mellitus
             compared with 10 equivalent untreated patients. In contrast
             to previous studies of patients with type II diabetes, no
             improvement occurred in glucose tolerance after 1 wk of
             intensive in-hospital relaxation training or in
             glycohemoglobin and total daily insulin dose after 6 wk of
             practicing relaxation techniques at home. This and other
             studies suggest that this type and amount relaxation therapy
             may not be as useful for enhancing blood glucose control in
             patients with type I diabetes as in those with type II
             diabetes. However, subpopulations of type I diabetic
             patients who have demonstrated stress-induced hyperglycemia
             should be further investigated.},
   Doi = {10.2337/diacare.10.1.72},
   Key = {fds276427}
}

@article{fds305772,
   Author = {MCCUBBIN, JA and SURWIT, RS and WILLIAMS, RB and NEMEROFF,
             CB},
   Title = {NALOXONE AND BLOOD-PRESSURE RESPONSES TO DIFFERENT TYPES OF
             STRESS},
   Journal = {Psychophysiology},
   Volume = {23},
   Number = {4},
   Pages = {451-451},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1986},
   Month = {July},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1986D953600140&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305772}
}

@article{fds305809,
   Author = {STABLER, B and SURWIT, RS and LANE, JD and MORRIS, MA and FEINGLOS,
             MN},
   Title = {GLYCEMIC RESPONSE TO STRESS IN CHILDREN WITH
             INSULIN-DEPENDENT DIABETES},
   Journal = {Psychophysiology},
   Volume = {23},
   Number = {4},
   Pages = {463-464},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1986},
   Month = {July},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1986D953600186&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305809}
}

@article{fds305798,
   Author = {SURWIT, RS and FEINGLOS, MN and COCHRANE, C and KUHN,
             CM},
   Title = {ALTERED ALPHA-ADRENERGIC RESPONSIVITY IN C576J
             MICE},
   Journal = {Diabetes},
   Volume = {35},
   Pages = {A19-A19},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1986},
   Month = {May},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1986C237100074&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305798}
}

@article{fds305810,
   Author = {STABLER, BS and MORRIS, MA and LITTON, J and FEINGLOS, MN and SURWIT,
             RS},
   Title = {TYPE-A BEHAVIOR PATTERN AND GLYCEMIC CONTROL IN
             IDDM},
   Journal = {Diabetes},
   Volume = {35},
   Pages = {A110-A110},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1986},
   Month = {May},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1986C237100435&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305810}
}

@article{fds276352,
   Author = {Surwit, RS and McCubbin, JA and Kuhn, CM and McGee, D and Gerstenfeld,
             D and Feinglos, MN},
   Title = {Alprazolam reduces stress hyperglycemia in ob/ob
             mice.},
   Journal = {Psychosomatic Medicine},
   Volume = {48},
   Number = {3-4},
   Pages = {278-282},
   Year = {1986},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2871583},
   Keywords = {Alprazolam • Animals • Anti-Anxiety Agents •
             Benzodiazepines • Blood Glucose • Diabetes
             Mellitus, Experimental • Hyperglycemia • Insulin
             • Mice • Mice, Inbred C57BL • Mice, Obese
             • Stress, Psychological • blood •
             complications* • drug therapy* • metabolism •
             therapeutic use*},
   Abstract = {We have shown that the C57BL/6J ob/ob (obese) mouse, a
             commonly used model of type II diabetes mellitus, is not in
             fact consistently hyperglycemic except when exposed to
             environmental stress. In an attempt to modify stress
             hyperglycemia in this animal, we administered either a 5
             mg/kg dose of the benzodiazepine alprazolam or vehicle
             (propylene glycol) intraperitoneally to both obese mice and
             their lean littermates prior to a rest and a stress period.
             Alprazolam modified the hyperglycemic effect of stress only
             in the obese mice. Alprazolam significantly reduced plasma
             corticosterone in obese animals at rest and following
             stress. In addition, alprazolam significantly increased
             plasma insulin in all animals at rest and following stress.
             These data suggest a possible role for benzodiazepines in
             the modification of stress hyperglycemia in type II diabetes
             mellitus.},
   Doi = {10.1097/00006842-198603000-00013},
   Key = {fds276352}
}

@article{fds276360,
   Author = {Stabler, B and Morris, MA and Litton, J and Feinglos, MN and Surwit,
             RS},
   Title = {Differential glycemic response to stress in type A and type
             B individuals with IDDM.},
   Journal = {Diabetes Care},
   Volume = {9},
   Number = {5},
   Pages = {550-552},
   Year = {1986},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3769723},
   Keywords = {Adolescent • Blood Glucose • Child • Diabetes
             Mellitus, Type 1 • Eating • Female • Humans
             • Male • Personality* • Stress, Psychological
             • Type A Personality* • blood • metabolism*
             • physiopathology* • psychology*},
   Doi = {10.2337/diacare.9.5.550b},
   Key = {fds276360}
}

@article{fds276397,
   Author = {Surwit, RS and McCubbin, JA and Livingston, EG and Feinglos,
             MN},
   Title = {Classically conditioned hyperglycemia in the obese
             mouse.},
   Journal = {Psychosomatic Medicine},
   Volume = {47},
   Number = {6},
   Pages = {565-568},
   Year = {1985},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4070525},
   Keywords = {Animals • Blood Glucose • Conditioning, Classical*
             • Diabetes Mellitus, Type 2 • Hyperglycemia •
             Mice • Mice, Obese • Stress, Psychological •
             analysis • blood • blood* •
             etiology*},
   Abstract = {The obese (C57BL/6J ob/ob) mouse is a commonly used animal
             model of non-insulin-dependent diabetes mellitus. It has
             recently been demonstrated that this mouse is not
             consistently hyperglycemic, however, unless it is subjected
             to environmental stress. In the present study, hyperglycemia
             in obese mice was induced by classical conditioning. Obese
             diabetic mice and lean control animals were exposed to
             shaking stress. All animals developed hyperglycemia in
             response to shaking. To demonstrate classical conditioning,
             some obese and lean animals were exposed to a metronome
             prior to and during the shaking. Other animals were exposed
             to the metronome and shaking in a noncontingent fashion and
             one group of animals was exposed to the metronome without
             any exposure to shaking. All animals received seven
             exposures to one of the three above conditions over a 3-day
             period. On the 4th day all animals were exposed to the
             metronome alone, following which blood samples were drawn.
             Classical conditioning of stress hyperglycemia was
             demonstrated in obese, but not in lean, mice.},
   Doi = {10.1097/00006842-198511000-00006},
   Key = {fds276397}
}

@article{fds276413,
   Author = {McCubbin, JA and Surwit, RS and Williams, RB},
   Title = {Endogenous opiate peptides, stress reactivity, and risk for
             hypertension.},
   Journal = {Hypertension},
   Volume = {7},
   Number = {5},
   Pages = {808-811},
   Year = {1985},
   ISSN = {0194-911X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4030048},
   Keywords = {Adolescent • Adult • Blood Pressure •
             Endorphins • Humans • Hypertension • Male
             • Naloxone • Risk • Stress, Psychological
             • complications* • etiology* • pharmacology
             • physiology*},
   Abstract = {Endogenous opiate peptides can regulate neuroendocrine and
             circulatory responses to behavioral stress and may be
             important in the pathogenic effects of sympathoadrenal
             reactivity. We tested this hypothesis by examining the
             effect of the opiate antagonist naloxone on blood pressure
             responses to behavioral stress in young adults with high,
             medium, or low casual blood pressures. Naloxone increased
             mean arterial pressure responses to stress in subjects with
             low casual pressure, but had no significant effect on
             responses in subjects with high casual pressure. These
             results suggest opioidergic inhibition of sympathetic
             nervous system responses may be deficient in persons at risk
             for essential hypertension.},
   Doi = {10.1161/01.hyp.7.5.808},
   Key = {fds276413}
}

@article{fds276358,
   Author = {Surwit, RS and Rotberg, M},
   Title = {Biofeedback therapy of essential blepharospasm.},
   Journal = {American Journal of Ophthalmology},
   Volume = {98},
   Number = {1},
   Pages = {28-31},
   Year = {1984},
   Month = {July},
   ISSN = {0002-9394},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6742078},
   Keywords = {Aged • Biofeedback (Psychology)* • Blepharospasm
             • Blinking • Electromyography • Eyelid
             Diseases • Female • Humans • Male •
             Middle Aged • physiopathology •
             therapy*},
   Abstract = {Eight patients with essential blepharospasm were given five
             consecutive sessions of electromyogram biofeedback from
             cutaneous electrodes placed over the frontalis muscle. Four
             of the eight patients demonstrated a 60% or greater
             reduction in blepharospasm frequency. Posttreatment
             electromyogram significantly predicted improvement of
             blepharospasm. These data suggest that electromyogram
             biofeedback may provide a therapeutic alternative to the
             treatment of this disabling condition.},
   Doi = {10.1016/0002-9394(84)90184-3},
   Key = {fds276358}
}

@article{fds276426,
   Author = {Surwit, RS and Feinglos, MN and Livingston, EG and Kuhn, CM and McCubbin, JA},
   Title = {Behavioral manipulation of the diabetic phenotype in ob/ob
             mice.},
   Journal = {Diabetes},
   Volume = {33},
   Number = {7},
   Pages = {616-618},
   Year = {1984},
   Month = {July},
   ISSN = {0012-1797},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6376217},
   Keywords = {Animals • Blood Glucose • Corticosterone •
             Diabetes Mellitus • Epinephrine • Handling
             (Psychology) • Insulin • Mice • Mice, Inbred
             C57BL • Mice, Obese • Phenotype • Restraint,
             Physical • Rodent Diseases • Stress • blood
             • blood* • metabolism* • pharmacology* •
             veterinary*},
   Abstract = {The genetically obese mouse (C57BL/6J ob/ob) is a commonly
             used model of non-insulin-dependent diabetes mellitus.
             However, our studies demonstrate that, while the animal is
             significantly hyperinsulinemic, it in fact does not show
             consistent hyperglycemia in the resting state. During
             stress, both obese animals and their lean littermates become
             hyperglycemic, but the magnitude of the hyperglycemia is
             exaggerated in the obese mice. Obese animals also show an
             exaggerated plasma glucose increase in response to
             epinephrine injection. This increase in plasma glucose is
             accompanied by a decrease in plasma insulin in response to
             both stress and epinephrine. Our findings suggest that
             environmental stimuli influence the expression of diabetes
             in the C57BL/6J obese mouse and therefore must be considered
             in studies of this animal model of diabetes.},
   Doi = {10.2337/diab.33.7.616},
   Key = {fds276426}
}

@article{fds276364,
   Author = {Surwit, RS and Gilgor, RS and Allen, LM and Duvic,
             M},
   Title = {A double-blind study of prazosin in the treatment of
             Raynaud's phenomenon in scleroderma.},
   Journal = {Archives of Dermatology},
   Volume = {120},
   Number = {3},
   Pages = {329-331},
   Year = {1984},
   Month = {March},
   ISSN = {0003-987X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6367665},
   Keywords = {Adult • Clinical Trials • Double-Blind Method
             • Female • Humans • Male • Middle Aged
             • Prazosin • Quinazolines • Raynaud Disease
             • Scleroderma, Systemic • complications •
             drug therapy* • therapeutic use*},
   Abstract = {Nineteen patients with Raynaud's phenomenon in conjunction
             with progressive systemic sclerosis were given either
             prazosin hydrochloride (1 mg orally three times a day) or a
             placebo for eight weeks, after which the treatment procedure
             was reversed for four weeks. Prazosin was shown to be
             effective in reducing both the frequency and the severity of
             vasospasm reported by the patients.},
   Doi = {10.1001/archderm.1984.01650390051010},
   Key = {fds276364}
}

@article{fds305773,
   Author = {MCCUBBIN, JA and SURWIT, RS and WILLIAMS, RB},
   Title = {STRESS REACTIVITY, ENDOGENOUS OPIATE PEPTIDES AND RISK FOR
             HYPERTENSION},
   Journal = {Psychophysiology},
   Volume = {21},
   Number = {5},
   Pages = {587-587},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1984},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1984TF32000101&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305773}
}

@article{fds305794,
   Author = {SURWIT, RS and MCCUBBIN, JA and GERSTENFELD, DA and MCGEE, DJ and FEINGLOS, MN},
   Title = {ALPRAZOLAM ATTENUATES STRESS-INDUCED HYPERGLYCEMIA},
   Journal = {Psychosomatic Medicine},
   Volume = {46},
   Number = {3},
   Pages = {287-287},
   Publisher = {WILLIAMS & WILKINS},
   Year = {1984},
   Month = {January},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1984SU35200016&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305794}
}

@article{fds276359,
   Author = {Surwit, RS and Feinglos, MN},
   Title = {Relaxation-induced improvement in glucose tolerance is
             associated with decreased plasma cortisol.},
   Journal = {Diabetes Care},
   Volume = {7},
   Number = {2},
   Pages = {203-204},
   Year = {1984},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6734387},
   Keywords = {Glucose Tolerance Test* • Humans • Hydrocortisone
             • Relaxation* • blood*},
   Doi = {10.2337/diacare.7.2.203},
   Key = {fds276359}
}

@article{fds276396,
   Author = {Surwit, RS and Gilgor, RS and Duvic, M and Allen, LM and Neal,
             JA},
   Title = {Intra-arterial reserpine for Raynaud's syndrome. Systemic
             reactions without therapeutic benefit.},
   Journal = {Archives of Dermatology},
   Volume = {119},
   Number = {9},
   Pages = {733-735},
   Publisher = {American Medical Association (AMA)},
   Year = {1983},
   Month = {September},
   ISSN = {0003-987X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6614959},
   Keywords = {Adult • Brachial Artery • Cardiac Output •
             Double-Blind Method • Female • Heart Rate •
             Humans • Injections, Intra-Arterial • Male •
             Middle Aged • Raynaud Disease • Reserpine •
             Skin Temperature • Stroke Volume • administration
             & dosage* • adverse effects • drug effects •
             drug effects* • drug therapy* • therapeutic
             use},
   Abstract = {Twenty-four patients classified as having Raynaud's disease
             or Raynaud's phenomenon were given bilateral brachial artery
             injections of reserpine or saline in a double-blind fashion.
             In the six weeks following injection, there was no
             indication that reserpine produced clinical improvement or
             changed vasomotor reactivity in the treated patients.
             However, intra-arterial reserpine did produce systemic
             cardiovascular effects lasting up to six weeks. It is
             concluded that intra-arterial reserpine as used in this
             study is an ineffective treatment for Raynaud's disease or
             Raynaud's phenomenon and may have significant adverse
             effects.},
   Doi = {10.1001/archderm.1983.01650330025008},
   Key = {fds276396}
}

@article{fds276409,
   Author = {Surwit, RS and Keefe, FJ},
   Title = {The blind leading the blind: problems with the
             "double-blind" design in clinical biofeedback
             research.},
   Journal = {Biofeedback and Self Regulation},
   Volume = {8},
   Number = {1},
   Pages = {1-8},
   Year = {1983},
   Month = {March},
   ISSN = {0363-3586},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6882807},
   Keywords = {Biofeedback (Psychology)* • Double-Blind Method •
             Humans • Raynaud Disease • Research • Skin
             Temperature • therapy*},
   Doi = {10.1007/BF01000531},
   Key = {fds276409}
}

@article{fds276389,
   Author = {Surwit, RS and Allen, LM and Gilgor, RS and Schanberg, S and Kuhn, C and Duvic, M},
   Title = {Neuroendocrine response to cold in Raynaud's
             syndrome.},
   Journal = {Life Sciences},
   Volume = {32},
   Number = {9},
   Pages = {995-1000},
   Year = {1983},
   Month = {February},
   ISSN = {0024-3205},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6600810},
   Keywords = {Antibodies, Antinuclear • Cold* • Female •
             Humans • Hydrocortisone • Norepinephrine •
             Raynaud Disease • Time Factors • analysis •
             blood • blood* • physiopathology*},
   Abstract = {Eleven patients with Raynaud's syndrome accompanied by
             monospecific IgG ANA, nine patients with Raynaud's syndrome
             in the absence of ANA, and nine normal volunteers were
             exposed to an ambient cold challenge during which time
             venous blood was continuously sampled. ANA negative patients
             were shown to have significantly higher levels of cortisol
             during a cold challenge than either ANA positive patients or
             normal controls, and exhibited significantly lower levels of
             plasma norepinephrine compared with normal controls. ANA
             positive patients did not differ significantly from normals
             in their neuroendocrine response to cold. It is suggested
             that the high plasma cortisol found in Raynaud's syndrome in
             the absence of ANA may be responsible for the vasospasticity
             in this group of patients.},
   Doi = {10.1016/0024-3205(83)90930-x},
   Key = {fds276389}
}

@article{fds305797,
   Author = {SURWIT, RS and FEINGLOS, MN},
   Title = {THE EFFECTS OF RELAXATION ON GLUCOSE-TOLERANCE},
   Journal = {Psychosomatic Medicine},
   Volume = {45},
   Number = {1},
   Pages = {83-83},
   Publisher = {WILLIAMS & WILKINS},
   Year = {1983},
   Month = {January},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1983QG57900032&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305797}
}

@article{fds305800,
   Author = {SURWIT, RS and FEINGLOS, MN and HASTEDT, P},
   Title = {THE EFFECTS OF RELAXATION ON GLUCOSE-TOLERANCE IN INSULIN
             DEPENDENT DIABETES},
   Journal = {Diabetes},
   Volume = {32},
   Pages = {A171-A171},
   Publisher = {AMER DIABETES ASSOC},
   Year = {1983},
   Month = {January},
   ISSN = {0012-1797},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1983QV86300645&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305800}
}

@article{fds276401,
   Author = {Surwit, RS and Feinglos, MN},
   Title = {The effects of relaxations on glucose tolerance in
             non-insulin-dependent diabetes.},
   Journal = {Diabetes Care},
   Volume = {6},
   Number = {2},
   Pages = {176-179},
   Year = {1983},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6343022},
   Keywords = {Adult • Aged • Blood Glucose • Body Weight
             • Diabetes Mellitus • Female • Glucose
             Tolerance Test • Humans • Insulin • Male
             • Middle Aged • Relaxation Techniques* •
             administration & dosage • analysis* • secretion
             • therapy*},
   Abstract = {Twelve patients with non-insulin-dependent diabetes mellitus
             were hospitalized on a clinical research ward under
             identical conditions. A 3-h glucose tolerance test and an
             intravenous insulin tolerance test were performed on each
             patient. Half of the patients were then given 5 days of
             progressive relaxation training after which all patients
             were retested while treated patients practiced relaxation.
             Relaxation was found to significantly improve glucose
             tolerance without affecting insulin sensitivity or
             glucose-stimulated insulin secretory activity.},
   Doi = {10.2337/diacare.6.2.176},
   Key = {fds276401}
}

@article{fds276414,
   Author = {Surwit, RS and Feinglos, MN and Scovern, AW},
   Title = {Diabetes and behavior: A paradigm for health
             psychology.},
   Journal = {American Psychologist},
   Volume = {38},
   Number = {3},
   Pages = {255-262},
   Publisher = {American Psychological Association (APA)},
   Year = {1983},
   ISSN = {0003-066X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6870041},
   Keywords = {Adaptation, Psychological • Blood Glucose •
             Diabetes Mellitus • Humans • Psychophysiologic
             Disorders • Sick Role* • metabolism •
             psychology*},
   Doi = {10.1037/0003-066x.38.3.255},
   Key = {fds276414}
}

@article{fds305807,
   Author = {Surwit, RS and Feinglos, MN and Livingston, EG and Kuhn, CM and McCubbin, JA},
   Title = {Stress and the expression of the diabetic phenotype in OB/OB
             mice},
   Journal = {Psychophysiology},
   Volume = {20},
   Number = {4},
   Pages = {474-474},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1983},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1983RF28200200&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305807}
}

@article{fds276371,
   Author = {Surwit, RS and Allen, LM and Gilgor, RS and Duvic,
             M},
   Title = {The combined effect of prazosin and autogenic training on
             cold reactivity in Raynaud's phenomenon.},
   Journal = {Biofeedback and Self Regulation},
   Volume = {7},
   Number = {4},
   Pages = {537-544},
   Year = {1982},
   Month = {December},
   ISSN = {0363-3586},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7165784},
   Keywords = {Adult • Autogenic Training* • Blood Pressure
             • Cold* • Female • Fingers • Humans
             • Male • Middle Aged • Prazosin •
             Quinazolines • Raynaud Disease • Scleroderma,
             Systemic • Skin • Skin Temperature • blood
             supply • complications • drug effects •
             therapeutic use* • therapy*},
   Doi = {10.1007/BF00998892},
   Key = {fds276371}
}

@article{fds276433,
   Author = {Surwit, RS},
   Title = {Behavioral treatment of Raynaud's syndrome in peripheral
             vascular disease.},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {50},
   Number = {6},
   Pages = {922-932},
   Year = {1982},
   Month = {December},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7174981},
   Keywords = {Behavior Therapy • Biofeedback (Psychology) •
             Humans • Muscle Relaxation • Prognosis •
             Raynaud Disease • methods* • psychology •
             therapy*},
   Doi = {10.1037//0022-006x.50.6.922},
   Key = {fds276433}
}

@article{fds276349,
   Author = {Steptoe, A and Surwit, R},
   Title = {Behavioral medicine},
   Journal = {Journal of Psychosomatic Research},
   Volume = {26},
   Number = {5},
   Pages = {467-468},
   Publisher = {Elsevier BV},
   Year = {1982},
   Month = {January},
   ISSN = {0022-3999},
   url = {http://dx.doi.org/10.1016/0022-3999(82)90085-X},
   Doi = {10.1016/0022-3999(82)90085-X},
   Key = {fds276349}
}

@article{fds276422,
   Author = {Surwit, RS and Scovern, AW and Feinglos, MN},
   Title = {The role of behavior in diabetes care.},
   Journal = {Diabetes Care},
   Volume = {5},
   Number = {3},
   Pages = {337-342},
   Year = {1982},
   ISSN = {0149-5992},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6756844},
   Keywords = {Autonomic Nervous System • Behavior* • Diabetes
             Mellitus • Humans • Life Style • Patient
             Compliance • Psychosomatic Medicine • Sympathetic
             Nervous System • physiopathology • psychology*
             • therapy},
   Abstract = {The treatment of people with diabetes mellitus almost always
             involves an effort on the part of the health-care team to
             impose new patterns of behavior on their patients. Too often
             this behavior modification is undertaken without any
             specific attention to factors in the treatment regimen that
             may enhance or detract from patient compliance. If, however,
             the treatment of disease is viewed in terms of changes in
             both physiology and behavior, the importance of intervention
             aimed at either direct behavioral manipulation of
             physiology, or alterations of secondary behavior related to
             the disease and its therapy, becomes apparent. We have
             reviewed in this paper the current "state of the art" of
             both direct behavioral treatment of diabetes and techniques
             to enhance compliance with treatment program.},
   Doi = {10.2337/diacare.5.3.337},
   Key = {fds276422}
}

@article{fds276366,
   Author = {Keefe, FJ and Block, AR and Williams, RB and Surwit,
             RS},
   Title = {Behavioral treatment of chronic low back pain: clinical
             outcome and individual differences in pain
             relief.},
   Journal = {Pain},
   Volume = {11},
   Number = {2},
   Pages = {221-231},
   Year = {1981},
   Month = {October},
   ISSN = {0304-3959},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6459557},
   Keywords = {Adult • Back Pain • Behavior Therapy •
             Biofeedback (Psychology) • Chronic Disease •
             Electromyography • Female • Humans •
             Individuality • MMPI • Male • Outcome and
             Process Assessment (Health Care) • Relaxation
             Techniques • methods* • psychology • therapy
             • therapy*},
   Abstract = {The response of 111 chronic low back pain patients to a
             comprehensive behavioral treatment program emphasizing
             relaxation procedures is examined. Over the course of
             treatment, significant reductions were obtained on measures
             of subjective tension, EMG activity, and pain. Many patients
             also decreased their intake of analgesic/narcotic agents and
             reported an increase in activity level. In order to examine
             individual differences in pain relief, the 28 patients who
             had the greatest decreases in pain were compared to those
             who had the least decreases in pain. Patients who had the
             best outcome in terms of pain relief were significantly more
             likely to show improvements in other outcome measures. In
             addition, these patients rated their pain initially as more
             severe, had continuous pain for fewer years, and were less
             likely to be on disability or to have had multiple surgical
             procedures. These results are discussed in the light of
             recent data from other behavioral treatment studies with
             chronic low back pain patients and implications for
             behavioral assessment and treatment are discussed.},
   Doi = {10.1016/0304-3959(81)90007-5},
   Key = {fds276366}
}

@article{fds276408,
   Author = {Rotberg, MH and Surwit, RS},
   Title = {Biofeedback techniques in the treatment of visual and
             ophthalmologic disorders: a review of the
             literature.},
   Journal = {Biofeedback and Self Regulation},
   Volume = {6},
   Number = {3},
   Pages = {375-388},
   Year = {1981},
   Month = {September},
   ISSN = {0363-3586},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7034790},
   Keywords = {Biofeedback (Psychology)* • Blepharospasm • Eye
             Diseases • Eye Movements • Female • Humans
             • Intraocular Pressure • Middle Aged • Myopia
             • Nystagmus, Pathologic • Oculomotor Muscles
             • Strabismus • Vision Disorders • Visual
             Acuity • physiology • therapy •
             therapy*},
   Abstract = {The literature on the use of biofeedback techniques in the
             treatment of visual and ophthalmologic disorders is
             reviewed. Although this consists mainly of case studies,
             there is mounting evidence that biofeedback may be
             applicable to the treatment of strabismus, nystagmus,
             blepharospasm, elevated intraocular pressure, and myopia.
             because of the success in applying biofeedback techniques in
             the treatment of other neuromuscular disorders, it is
             concluded that the use of these techniques in the treatment
             of blepharospasm and strabismus shows the most
             promise.},
   Doi = {10.1007/BF01000662},
   Key = {fds276408}
}

@article{fds276375,
   Author = {Keefe, FJ and Surwit, RS and Pilon, RN},
   Title = {Collagen vascular disease: can behavior therapy
             help?},
   Journal = {Journal of Behavior Therapy and Experimental
             Psychiatry},
   Volume = {12},
   Number = {2},
   Pages = {171-175},
   Year = {1981},
   Month = {June},
   ISSN = {0005-7916},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7276192},
   Keywords = {Autogenic Training • Behavior Therapy •
             Biofeedback (Psychology) • Body Temperature Regulation
             • Female • Humans • Middle Aged • Mixed
             Connective Tissue Disease • Raynaud Disease •
             methods* • psychology • therapy*},
   Abstract = {This study examined the efficacy of a simple autogenic and
             biofeedback treatment package in the management of Raynaud's
             Phenomenon secondary to diagnosed collagen vascular disease.
             The patient, diagnosed as suffering from mixed connective
             tissue disease, had an average of 6.3 vasospastic attacks
             per day during a 2 week baseline period. The frequency of
             daily attacks dropped to 4.2 after 10 weeks and 2.5 attacks
             after 1 yr of training. In addition, the patient displayed a
             gradual improvement in the ability to maintain digital skin
             temperature in the presence of ambient cold
             stress.},
   Doi = {10.1016/0005-7916(81)90013-6},
   Key = {fds276375}
}

@article{fds305791,
   Author = {SURWIT, RS and ALLEN, LM and KUHN, CM and GILGOR, RS and DUVIC, M and SCHANBERG, SM and WILLIAMS, RB},
   Title = {NEUROENDOCRINE CORRELATES OF RAYNAUDS DISEASE AND RAYNAUD
             PHENOMENON},
   Journal = {Psychophysiology},
   Volume = {18},
   Number = {2},
   Pages = {204-204},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1981},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1981LH49500214&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305791}
}

@article{fds305774,
   Author = {SURWIT, RS},
   Title = {INDIVIDUAL-DIFFERENCES IN RESPONSE TO THE BEHAVIORAL
             TREATMENT OF RAYNAUD DISEASE},
   Journal = {Psychophysiology},
   Volume = {18},
   Number = {2},
   Pages = {200-201},
   Publisher = {SOC PSYCHOPHYSIOL RES},
   Year = {1981},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1981LH49500203&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305774}
}

@article{fds276404,
   Author = {Surwit, RS},
   Title = {Behavioral approaches to Raynaud's disease.},
   Journal = {Psychotherapy and Psychosomatics},
   Volume = {36},
   Number = {3-4},
   Pages = {224-245},
   Year = {1981},
   ISSN = {0033-3190},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7345469},
   Keywords = {Adult • Arousal • Autogenic Training •
             Behavior Therapy • Biofeedback (Psychology) •
             Female • Humans • Outcome and Process Assessment
             (Health Care) • Raynaud Disease • Skin • Skin
             Temperature • Vasoconstriction • Vasodilation
             • blood supply • methods* • psychology •
             therapy*},
   Doi = {10.1159/000287546},
   Key = {fds276404}
}

@article{fds305782,
   Author = {Surwit, RS},
   Title = {Evaluation of Clinical Biofeedback},
   Journal = {Psychosomatic Medicine},
   Volume = {42},
   Number = {3},
   Pages = {379-380},
   Publisher = {Ovid Technologies (Wolters Kluwer Health)},
   Year = {1980},
   Month = {May},
   ISSN = {0033-3174},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1980KP45700009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Doi = {10.1097/00006842-198005000-00012},
   Key = {fds305782}
}

@article{fds276416,
   Author = {Surwit, RS and Fenton, CH},
   Title = {Feedback and instructions in the control of digital skin
             temperature.},
   Journal = {Psychophysiology},
   Volume = {17},
   Number = {2},
   Pages = {129-132},
   Year = {1980},
   Month = {March},
   ISSN = {0048-5772},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7375614},
   Keywords = {Adult • Biofeedback (Psychology)* • Female •
             Fingers • Humans • Middle Aged • Raynaud
             Disease • Skin Temperature* • therapy*},
   Doi = {10.1111/j.1469-8986.1980.tb00123.x},
   Key = {fds276416}
}

@article{fds276348,
   Author = {Surwit, RS},
   Title = {Biofeedback training in clinical cardiovascular
             disease},
   Journal = {Primary Cardiology},
   Volume = {6},
   Number = {9},
   Pages = {34-48},
   Year = {1980},
   Month = {January},
   Abstract = {Biofeedback mechanisms have been shown to be effective in
             treating mild hypertension. Various forms include binary
             feedback training to lower blood pressure and heart rate,
             analogue feedback to control forearm and frontalis
             electromyographic activity, and meditation-relaxation
             procedures. The simple technique of having the patient take
             his own blood pressure and consciously attempt to lower it
             by whatever mechanism he can is quite effective. Thermal
             feedback training to control migraine headaches and
             Raynaud's disease has been successful. Autogenic training to
             control skin temperature is also an effective
             instrument.},
   Key = {fds276348}
}

@article{fds305783,
   Author = {SURWIT, RS and GILGOR, RS and DUVIC, M and WILLIAMS, R and SCHANBERG, S and NEAL, J},
   Title = {RAYNAUDS DISEASE - ROLE OF THE AUTONOMIC NERVOUS-SYSTEM IN
             PATHOGENESIS},
   Journal = {Journal of Investigative Dermatology},
   Volume = {75},
   Number = {5},
   Pages = {459-459},
   Publisher = {BLACKWELL SCIENCE INC},
   Year = {1980},
   Month = {January},
   ISSN = {0022-202X},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1980KQ62500019&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305783}
}

@article{fds276353,
   Author = {Keefe, FJ and Surwit, RS and Pilon, RN},
   Title = {Biofeedback, autogenic training, and progressive relaxation
             in the treatment of Raynaud's disease: a comparative
             study.},
   Journal = {Journal of Applied Behavior Analysis},
   Volume = {13},
   Number = {1},
   Pages = {3-11},
   Year = {1980},
   ISSN = {0021-8855},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6988380},
   Keywords = {Autogenic Training* • Biofeedback (Psychology)* •
             Cold • Female • Heart Rate • Humans •
             Raynaud Disease • Relaxation Techniques* • Skin
             Temperature • therapy*},
   Abstract = {Twenty-one female patients suffering from diagnosed
             idiopathic Raynaud's Disease were trained to raise digital
             skin temperature using either autogenic training,
             progressive muscle relaxation, or a combination of autogenic
             training and skin temperature feedback. Patients were
             instructed in the treatment procedures in three one-hour
             group sessions spaced one week apart. All patients were
             instructed to practice what they had learned twice a day at
             home. Patients kept records of the frequency of vasospastic
             attacks occurring over a four-week baseline period, and
             during the first four weeks and the ninth week of training.
             In addition, patients underwent four laboratory cold stress
             tests during which they were instructed to maintain digital
             temperature as the ambient temperature was slowly dropped
             from 26 degrees to 17 degrees C. Cold stress tests were
             given during week 1 of baseline and during weeks 1, 3, and 5
             of training. No significant differences between the three
             behavioral treatment procedures were obtained. In addition,
             the ability of patients to maintain digital temperature
             during the cold stress challenge showed significant
             improvement from the first to the last tests. Symptomatic
             improvement was maintained by all patients nine weeks after
             the start of training. The implications of these findings
             for the behavioral treatment of Raynaud's Disease are
             discussed.},
   Doi = {10.1901/jaba.1980.13-3},
   Key = {fds276353}
}

@article{fds276400,
   Author = {Keefe, FJ and Surwit, RS and Pilon, RN},
   Title = {A 1-year follow-up of Raynaud's patients treated with
             behavioral therapy techniques.},
   Journal = {Journal of Behavioral Medicine},
   Volume = {2},
   Number = {4},
   Pages = {385-391},
   Year = {1979},
   Month = {December},
   ISSN = {0160-7715},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/548581},
   Keywords = {Adult • Autogenic Training* • Biofeedback
             (Psychology)* • Female • Fingers • Heart Rate
             • Humans • Middle Aged • Raynaud Disease
             • Skin Temperature • diagnosis •
             therapy*},
   Abstract = {The purpose of this study was to assess to what degree
             learned control of digital temperature and vasospastic
             attacks can be retained by Raynaud's patients over a full
             year period. Subjects were 19 patients suffering from
             diagnosed idiopathic Raynaud's disease who had undergone
             behavioral training. These patients had been trained to
             increase digital temperature using either autogenic
             training, biofeedback, or a combination of autogenic
             training and temperature biofeedback. Results indicated that
             the mean number of vasospastic attacks per day occurring 1
             year after training was approximately equal to the number
             occurring at the end of the initial training (1.2-1.3 per
             day). Patient satisfaction with the treatment program was
             above average (3.5 on a 5-point scale). The patients'
             ability to maintain digital temperature during the cold
             stress challenge was imparied, however. At 1-year follow-up,
             digital temperature readings taken in the laboratory were
             identical to baseline levels.},
   Doi = {10.1007/BF00844742},
   Key = {fds276400}
}

@article{fds276355,
   Author = {Surwit, RS and Bradner, MN and Fenton, CH and Pilon,
             RN},
   Title = {Individual differences in response to the behavioral
             treatment of Raynaud's disease.},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {47},
   Number = {2},
   Pages = {363-367},
   Year = {1979},
   Month = {April},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/469084},
   Keywords = {Adult • Autogenic Training • Behavior Therapy
             • Female • Humans • Individuality* •
             Middle Aged • Raynaud Disease • Skin Temperature
             • methods* • psychology •
             therapy*},
   Doi = {10.1037//0022-006x.47.2.363},
   Key = {fds276355}
}

@article{fds305781,
   Author = {SURWIT, RS and FENTON, CH},
   Title = {ROLE OF VISUAL TEMPERATURE IN VOLUNTARY DIGITAL TEMPERATURE
             AUTO-REGULATION},
   Journal = {Psychophysiology},
   Volume = {16},
   Number = {2},
   Pages = {187-188},
   Publisher = {CAMBRIDGE UNIV PRESS},
   Year = {1979},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1979GN13600066&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305781}
}

@article{fds305780,
   Author = {SURWIT, RS},
   Title = {BIOFEEDBACK - PRINCIPLES AND PRACTICE FOR CLINICIANS -
             BASMAJIAN,JV},
   Journal = {Contemporary Psychology: a Journal of Reviews},
   Volume = {24},
   Number = {10},
   Pages = {810-811},
   Publisher = {AMER PSYCHOLOGICAL ASSOC},
   Year = {1979},
   Month = {January},
   ISSN = {0010-7549},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1979HT09600058&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305780}
}

@article{fds276392,
   Author = {Surwit, RS and Pilon, RN and Fenton, CH},
   Title = {Behavioral treatment of Raynaud's disease.},
   Journal = {Journal of Behavioral Medicine},
   Volume = {1},
   Number = {3},
   Pages = {323-335},
   Year = {1978},
   Month = {September},
   ISSN = {0160-7715},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/755865},
   Keywords = {Adult • Autogenic Training • Behavior Therapy
             • Biofeedback (Psychology) • Cold • Female
             • Generalization, Response • Humans • Middle
             Aged • Raynaud Disease • Skin Temperature •
             methods* • psychology • therapy*},
   Abstract = {In order to assess the efficacy of a behavioral intervention
             in the treatment of idiopathic Raynaud's disease, 30 female
             patients were trained to control their digital skin
             temperature using autogenic training or a combination of
             autogenic training and skin temperature feedback either in
             the laboratory or at home. All trained subjects demonstrated
             a significant ability to maintain digital skin temperature
             in the presence of a cold stress challenge and reported
             significant reductions in both frequency and intensity of
             vasospastic attacks. The addition of skin temperature
             feedback to autogenic training did not provide additional
             clinical benefit.},
   Doi = {10.1007/BF00846683},
   Key = {fds276392}
}

@article{fds276394,
   Author = {Hager, JL and Surwit, RS},
   Title = {Hypertension self-control with a portable feedback unit or
             meditation-relaxation.},
   Journal = {Biofeedback and Self Regulation},
   Volume = {3},
   Number = {3},
   Pages = {269-276},
   Year = {1978},
   Month = {September},
   ISSN = {0363-3586},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/365249},
   Keywords = {Adult • Biofeedback (Psychology)* • Blood Pressure
             • Blood Pressure Determination • Female •
             Humans • Hypertension • Male • Relaxation
             Techniques* • instrumentation* •
             therapy*},
   Abstract = {Thirty borderline essential hypertensives were randomly
             assigned to a portable constant-cuff blood pressure feedback
             technique or meditation-relaxation. Each technique was
             taught in the laboratory, then practiced twice daily at home
             for four weeks. Subjects mailed daily records of their
             progress. Seven feedback and ten meditation-relaxation
             subjects completed the program. Both techniques produced
             significant systolic and diastolic reductions within
             practice sessions and diastolic reductions over weeks of
             training. Neither technique improved reductions nor reduced
             initial systolic pressure levels over the four weeks.
             Differences between biofeedback and meditation-relaxation in
             within-session pressure reductions were not
             significant.},
   Doi = {10.1007/BF00999295},
   Key = {fds276394}
}

@article{fds276368,
   Author = {Surwit, RS and Bradner, MN and Fenton, CH and Pilon,
             RN},
   Title = {Laterality of body focus and digital skin temperature in
             patients with Raynaud's disease.},
   Journal = {Psychophysiology},
   Volume = {15},
   Number = {4},
   Pages = {320-323},
   Year = {1978},
   Month = {July},
   ISSN = {0048-5772},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/693739},
   Keywords = {Adult • Body Image* • Female • Functional
             Laterality • Hand • Humans • Middle Aged
             • Raynaud Disease • Skin Temperature* •
             Vasomotor System • blood supply • physiology*
             • physiopathology • psychology*},
   Doi = {10.1111/j.1469-8986.1978.tb01386.x},
   Key = {fds276368}
}

@article{fds276388,
   Author = {Surwit, RS and Shapiro, D and Good, MI},
   Title = {Comparison of cardiovascular biofeedback, neuromuscular
             biofeedback, and meditation in the treatment of borderline
             essential hypertension.},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {46},
   Number = {2},
   Pages = {252-263},
   Year = {1978},
   Month = {April},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/348731},
   Keywords = {Adult • Biofeedback (Psychology)* • Blood Pressure
             • Electromyography • Female • Heart Rate
             • Humans • Hypertension • Male • Methods
             • Middle Aged • Relaxation Techniques* •
             therapy*},
   Doi = {10.1037//0022-006x.46.2.252},
   Key = {fds276388}
}

@article{fds276406,
   Author = {Keefe, FJ and Surwit, RS},
   Title = {Electromyographic biofeedback: behavioral treatment of
             neuromuscular disorders.},
   Journal = {Journal of Behavioral Medicine},
   Volume = {1},
   Number = {1},
   Pages = {13-24},
   Year = {1978},
   Month = {March},
   ISSN = {0160-7715},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/556109},
   Keywords = {Behavior Therapy • Biofeedback (Psychology)* •
             Bruxism • Cerebral Infarction • Electromyography
             • Humans • Neuromuscular Diseases • Outcome
             and Process Assessment (Health Care) • Poliomyelitis
             • Temporomandibular Joint Dysfunction Syndrome •
             Torticollis • Trauma, Nervous System • methods*
             • therapy • therapy*},
   Abstract = {Electromyographic biofeedback is becoming widely used to
             help patients regain voluntary control of specific muscles
             affected by neuromuscular disorders. Electromyographic
             feedback training has been employed in the rehabilitation of
             patients affected by poliomyelitis, cerebrovascular
             accident, torticollis, nerve injury, temporomandibular joint
             syndrome, bruxism, and other disorders. While EMG
             biofeedback appears to be a promising treatment technique,
             the research literature on its effectiveness consists mainly
             of uncontrolled case reports and clinical trials. It is
             concluded that new studies with more sophisticated design
             and more careful control are needed to demonstrate that EMG
             biofeedback makes a unique contribution to the treatment of
             neuromuscular disorders. Research is needed to identify
             relevant patients characteristics predictive of success,
             specify appropriate muscle groups for the treatment of
             particular disorders, determine how feedback can be most
             efficiently combined with more conventional techniques in
             achieving a therapeutic effect, and establish meaningful
             criteria of success in the treatment of neuromuscular
             disorders.},
   Doi = {10.1007/BF00846583},
   Key = {fds276406}
}

@article{fds276350,
   Author = {Surwit, RS and Keefe, FJ},
   Title = {Frontalis EMG feedback training: An electronic
             panacea?},
   Journal = {Behavior Therapy},
   Volume = {9},
   Number = {5},
   Pages = {779-792},
   Publisher = {Elsevier BV},
   Year = {1978},
   Month = {January},
   ISSN = {0005-7894},
   url = {http://dx.doi.org/10.1016/S0005-7894(78)80008-2},
   Abstract = {Studies dealing with the application of frontalis EMG
             feedback to the treatment of a variety of disorders are
             reveiwed. Successful applications of frontalis EMG feedback
             training have been reported in the treatment of muscle
             contraction headaches, asthma, essential hypertension,
             insomnia, chronic anxiety, phobias, and cerebral palsy.
             While available evidence does suggest that frontalis EMG
             feedback training may be helpful in the treatment of these
             disorders, these effects are equivalent but not superior to
             those that can be obtained using more conventional and less
             costly treatment techniques such as relaxation training. In
             addition, there appears to be a lack of clear rationale for
             the use of frontalis as a training site in treatment of
             these disorders. It is concluded that claims made about the
             clinical advantages of frontalis EMG biofeedback as compared
             to other methods of relaxation are not scientifically
             justified. © 1978 Association for Advancement of Behavior
             Therapy.},
   Doi = {10.1016/S0005-7894(78)80008-2},
   Key = {fds276350}
}

@article{fds305770,
   Author = {SURWIT, RS and PILON, RN and FENTON, CH},
   Title = {BEHAVIORAL TREATMENT OF RAYNAUD DISEASE},
   Journal = {Psychophysiology},
   Volume = {15},
   Number = {3},
   Pages = {286-286},
   Publisher = {CAMBRIDGE UNIV PRESS},
   Year = {1978},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1978FB62300100&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305770}
}

@article{fds305775,
   Author = {SURWIT, RS},
   Title = {WARMING THOUGHTS FOR A COLD WINTER},
   Journal = {Psychology Today},
   Volume = {12},
   Number = {7},
   Pages = {112-&},
   Publisher = {PSYCHOLOGY TODAY},
   Year = {1978},
   Month = {January},
   ISSN = {0033-3107},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1978FY51300042&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305775}
}

@article{fds276412,
   Author = {Surwit, RS},
   Title = {Simple versus complex feedback displays in the training of
             digital temperature.},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {45},
   Number = {1},
   Pages = {146-147},
   Year = {1977},
   Month = {February},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/845299},
   Keywords = {Acoustic Stimulation • Adolescent • Adult •
             Biofeedback (Psychology)* • Fingers • Humans
             • Male • Photic Stimulation • Reward •
             Skin Temperature* • physiology*},
   Doi = {10.1037//0022-006x.45.1.146},
   Key = {fds276412}
}

@article{fds305785,
   Author = {HAGER, JL and SURWIT, RS},
   Title = {HYPERTENSION SELF-CONTROL WITH A PORTABLE FEEDBACK UNIT OR
             RELAXATION},
   Journal = {Psychophysiology},
   Volume = {14},
   Number = {1},
   Pages = {97-98},
   Publisher = {CAMBRIDGE UNIV PRESS},
   Year = {1977},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1977CU63200079&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305785}
}

@article{fds305771,
   Author = {SURWIT, RS and HAGER, JL and FELDMAN, T},
   Title = {ROLE OF FEEDBACK IN VOLUNTARY CONTROL OF BLOOD-PRESSURE IN
             INSTRUCTED SUBJECTS},
   Journal = {Psychophysiology},
   Volume = {14},
   Number = {1},
   Pages = {97-97},
   Publisher = {CAMBRIDGE UNIV PRESS},
   Year = {1977},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:A1977CU63200078&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds305771}
}

@article{fds276395,
   Author = {Surwit, RS and Hager, JL and Feldman, T},
   Title = {The role of feedback in voluntary control of blood pressure
             in instructed subjects.},
   Journal = {Journal of Applied Behavior Analysis},
   Volume = {10},
   Number = {4},
   Pages = {625-631},
   Year = {1977},
   ISSN = {0021-8855},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/599107},
   Keywords = {Adolescent • Adult • Autogenic Training* •
             Biofeedback (Psychology)* • Blood Pressure* •
             Humans • Male • Methods • Reinforcement
             (Psychology) • Teaching},
   Abstract = {Forty normal male volunteers were randomly assigned to one
             of four experimental conditions and instructed to raise and
             lower their systolic blood pressure. Subjects received
             either beat-to-beat feedback contingent on pressure changes,
             noncontingent beat-to-beat feedback, noncontingent feedback
             presented randomly with respect to the occurrence of each
             heart beat, or instructions alone. The order of increase and
             decrease trial blocks was counterbalanced across groups.
             Subjects receiving contingent feedback were monetarily
             rewarded for appropriate pressure changes. Subjects
             receiving noncontingent feedback received rewards and
             feedback equal to the mean received by the contingent group.
             Subjects in the instructions-only condition were also paid
             this bonus but were informed of their earnings only at the
             conclusion of the experiment. Results indicated that in the
             presence of instructions, feedback, whether contingent or
             noncontingent, added little to subjects' ability to control
             pressure during a single session. Theoretical and clinical
             implications are discussed.},
   Doi = {10.1901/jaba.1977.10-625},
   Key = {fds276395}
}

@article{fds276411,
   Author = {SURWIT, RS and SHAPIRO, D},
   Title = {DIGITAL TEMPERATURE AUTOREGULATION AND ASSOCIATED
             CARDIOVASCULAR CHANGES},
   Journal = {Psychophysiology},
   Volume = {13},
   Number = {2},
   Pages = {165-165},
   Publisher = {CAMBRIDGE UNIV PRESS},
   Year = {1976},
   Month = {January},
   ISSN = {0048-5772},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1273229},
   Keywords = {Adolescent • Adult • Conditioning, Operant •
             Feedback • Female • Functional Laterality •
             Heart Rate* • Humans • Male • Pulse •
             Respiration • Reward • Sex Factors • Skin
             Temperature* • Temperature • physiology*},
   Doi = {10.1111/j.1469-8986.1976.tb00106.x},
   Key = {fds276411}
}

@article{fds276402,
   Author = {Surwit, RS and Poser, EG},
   Title = {Latent inhibition in the conditioned electrodermal
             response.},
   Journal = {Journal of Comparative and Physiological
             Psychology},
   Volume = {86},
   Number = {3},
   Pages = {543-548},
   Year = {1974},
   Month = {March},
   ISSN = {0021-9940},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4814770},
   Keywords = {Acoustic Stimulation • Adolescent • Adult •
             Animals • Attention • Conditioning, Classical*
             • Electroshock • Female • Galvanic Skin
             Response* • Humans • Inhibition (Psychology)*
             • Orientation • Photic Stimulation •
             Psychological Theory • Reaction Time • Research
             Design • Time Factors},
   Doi = {10.1037/h0036133},
   Key = {fds276402}
}

@article{fds276421,
   Author = {Shapiro, D and Surwit, RS},
   Title = {Operant conditioning: a new theoretical approach in
             psychosomatic medicine.},
   Journal = {International Journal of Psychiatry in Medicine},
   Volume = {5},
   Number = {4},
   Pages = {377-387},
   Year = {1974},
   ISSN = {0091-2174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4618839},
   Keywords = {Autogenic Training • Autonomic Nervous System •
             Behavior Therapy* • Conditioning, Operant* •
             Feedback • Generalization (Psychology) • Headache
             • Heart Rate • Humans • Hypertension •
             Motivation • Muscle Contraction • Paralysis •
             Psychophysiologic Disorders • Psychophysiology •
             Relaxation • Transfer (Psychology) • Yoga •
             physiology • rehabilitation • therapy •
             therapy*},
   Doi = {10.2190/7EYM-L28K-FT5C-AG07},
   Key = {fds276421}
}

@article{fds276424,
   Author = {Surwit, RS},
   Title = {Biofeedback: a possible treatment for Raynaud's
             disease.},
   Journal = {Seminars in Psychiatry},
   Volume = {5},
   Number = {4},
   Pages = {483-490},
   Year = {1973},
   Month = {November},
   ISSN = {0037-1971},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4770576},
   Keywords = {Adolescent • Adult • Autonomic Nervous System
             • Conditioning, Operant* • Feedback* • Female
             • Humans • Male • Middle Aged •
             Psychophysiologic Disorders • Raynaud Disease •
             Remission, Spontaneous • Skin Temperature •
             physiology • surgery • therapy •
             therapy*},
   Key = {fds276424}
}

@article{fds305764,
   Author = {Finch, DM and Surwit, RS and Johnson, RR},
   Title = {The effects of amygdalectomy on shock-induced fighting
             behavior in rats},
   Journal = {Psychonomic Science},
   Volume = {10},
   Number = {11},
   Pages = {369-370},
   Publisher = {Springer Nature},
   Year = {1968},
   Month = {January},
   ISSN = {0033-3131},
   url = {http://dx.doi.org/10.3758/BF03331565},
   Abstract = {Amygdaloid lesioned rats were compared to cortically
             lesioned and normal rats in their level of shock-induced
             fighting behavior. The resultant fighting scores, as rated
             on a four point scale, showed no significant difference in
             aggressive behavior on the part of the amygdalectomized
             group as compared to the cortical and normal control groups.
             Theoretical explanations of the results are proposed. ©
             1968, Psychonomic Journals. All rights reserved.},
   Doi = {10.3758/BF03331565},
   Key = {fds305764}
}


%% Chapters in Books   
@misc{fds366620,
   Author = {Surwit, RS},
   Title = {Glycemic responsivity to adrenergic stimulation and genetic
             predisposition to type II diabetes},
   Pages = {235-248},
   Booktitle = {Stress and Disease Processes: Perspectives in Behavioral
             Medicine},
   Year = {2018},
   Month = {January},
   ISBN = {0805811613},
   url = {http://dx.doi.org/10.4324/9781315827490-13},
   Abstract = {Since the 1980s, great strides have been made in the
             understanding of pathophysiology at the molecular level.
             Reverse genetic methods have been used to identify the
             mechanisms by which genetic defects cause a cascade of
             biochemical events leading to the development of disease.
             The promise of the molecular genetics has overshadowed much
             of the importance of conventional physiology and has shifted
             the focus of many scientists from the whole organism to
             microparticles. However, it is important to realize that
             ultimate potential of the molecular approach depends on a
             thorough understanding of how the organism functions in its
             environment. The reverse genetic methodology of molecular
             biology utilizes conventional genetics to map, localize, and
             clone genes related to disease. This approach is limited by
             our ability to identify individuals who show the phenotype
             of a particular disease. Diseases with "variable penetrance"
             are difficult to study genetically because the phenotype may
             not always be present in individuals who carry the genotype.
             One important lesson to come from behavioral medicine
             research is that many disease phenotypes result from the
             interaction of environmental stress and genetic
             predisposition. Acting through neuroendocrine pathways,
             stress disturbs the function of vulnerable end organ systems
             in predisposed individuals. This disturbance, if chronic,
             can lead to a permanent breakdown in function.},
   Doi = {10.4324/9781315827490-13},
   Key = {fds366620}
}


Duke University * Arts & Sciences * Faculty * Staff * Grad * Postdocs * Reload * Login