Nutrition & Food Science
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Item High Sucrose, Fructose, and Glucose Diets and Glucocorticoid Dysregulation in Rats(2009) London, Edra; Castonguay, Thomas W; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Approximately two-thirds of U.S. adults are overweight or obese and the prevalence of overweight in children has tripled since 1980. Intake of added sugars has also increased. The etiology of obesity remains unclear and the role of glucocorticoids in obesity is one area of ambiguity. The enzyme 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) interconverts active and inactive glucocorticoid, thereby regulating intracellular glucocorticoids. Dysregulation of 11beta-HSD-1 in liver and adipose is characteristic of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is colocalized with 11beta-HSD-1 and determines the set point for 11beta-HSD-1 oxidoreductase activity. In a long-term (10 wk) study, rats given ad libitum access to 16% sucrose solution, chow, and water were fatter than controls, had increased 11beta-HSD-1 mRNA in adipose, suppressed 11beta-HSD-1 mRNA in liver, and increased H6PDH mRNA in both tissues. The primary research questions were as follows: Can high sugar diets induce glucocorticoid dysregulation in the absence of excess adiposity? Does sugar type matter? Energy intake, weight gain, and parameters of lipid and carbohydrate metabolism were measured. Rats were randomly assigned to either ad libitum access to chow and water only (control), or in addition to ad libitum access to either 16% sucrose, fructose, or glucose solution (n=16/gp). After 24h and 1 wk, eight rats per group were randomly selected for sacrifice. Daily caloric intakes among sugar-fed groups did not differ and were higher than the mean intake of the control group. Within 24h, fructose induced increased 11beta-HSD-1 message in mesenteric adipose and liver. Plasma TG and insulin were acutely increased in groups with fructose-containing diets only. All high sugar diets induced suppressed hepatic 11beta-HSD-1 mRNA and protein after 1 wk. Upregulation of H6PDH mRNA observed in response to long-term high sucrose diets may result from increased adiposity and not solely diet. High sugar diets, irrespective of sugar type, initiate glucocorticoid dysregulation in the absence of phenotypic changes associated with obesity. Sucrose, fructose, and glucose have distinct metabolic and endocrine responses. Fructose has the unique ability to induce glucocorticoid dysregulation in liver and adipose in 24h.Item The Relationship of Low Birth Weight and Current Obesity to Diabetes in African-American Women(2007-04-26) Harris, B. Michelle; Lei, David K. Y.; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Aims: (1) To test the fetal origins of chronic disease by examining birth weight, current obesity, and odds of developing type 2 diabetes (T2DM) in African-American women 38-57 years. (2) To assess birth weight and obesity in relation to fasting plasma glucose (FPG). Background: African-American women suffer disproportionately in prevalence and complications of T2DM. According to the fetal origins of chronic disease, T2DM is related to low birth weight with subsequent adult obesity. Several studies have substantiated this hypothesis; none have focused on African-American women. Outcome Measure: Self-reported physician diagnosis of T2DM. Exposure Measures: Birth weight, an indicator for fetal growth; waist-to-hip ratio, a marker for abdominal obesity. Other factors: physical activity, body mass index (BMI), history of gestational diabetes, blood pressure. Design: Retrospective, case-control observational study. Method: Convenience sample of urban African-American women. Cases (n=95) reported a physician diagnosis of T2DM. Controls (n=186), matched on race and age, reported no T2DM diagnosis. To verify control status, participants were screened for elevated FPG (cut-point, <126>mg/dL, as defined by the American Diabetes Association). Vital and family records were sources for birth weight. Current weight, height, and waist and hip circumferences were measured; BMI and waist-to-hip ratio were calculated. Confounding factors were collected on a 68-item questionnaire. Logistic regression analysis tested the proposed model for the odds of having T2DM. Multiple linear regression analysis was employed to assess FPG. Sample size was estimated. Results: The odds ratio for T2DM increased as waist-to-hip ratio increased (OR=1.13, 95% CI=1.08, 1.19, p<.0001). Birth weight did not contribute independently to the model's ability to examine T2DM (OR=0.92, 95% CI=0.74, 1.14, p=.4409). Birth weight and waist-to-hip ratio each contributed independently to assessing FPG. Conclusions: This study found an interaction between birth weight and abdominal obesity when examining T2DM in African-American women: those born small and who subsequently developed abdominal obesity had a greater odds for T2DM. Abdominal obesity, but not birth weight, was independently associated with T2DM. FPG significantly increased with increasing abdominal obesity and decreasing birth weight. African-American women are cautioned to maintain healthy body measures (waist-to-hip ratio <0.80 and BMI <25) to address T2DM.Item Evaluating the Effects of Weight Loss on Exercise-Induced Oxidative Stress in Obese/Overweight Soliders(2006-08-03) Andrews, Anne; Kantor, Mark A; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Exercise is known to increase reactive oxygen species, a condition recognized as oxidative stress. Obese individuals may experience even greater amounts of oxidative stress after exercise compared to normal weight people. It is not clear how weight loss affects exercise-induced oxidative stress in overweight subjects. The objectives of this study were to 1) evaluate the effect of the Army Physical Fitness Test (APFT) on biomarkers of oxidative stress in overweight/obese soldiers 2) determine the effects of dietary antioxidants, fitness level, body composition on exercise-induced oxidative stress, and 3) determine the effect of weight loss on changes in biomarkers of oxidative stress as a result of the APFT. A total of 60 subjects (35 M, 25 F) were recruited. After completing the 1st APFT (n=47), subjects followed a 3-month weight loss program and then completed the 2nd APFT (n=29). Blood measurements of the oxidative stress biomarkers creatine kinase (CK), C-reactive protein (CRP), glutathione peroxidase (GPX), and superoxide dismutase (SOD) were taken pre, immediately after and 24hrs after each exercise test. Dietary antioxidant intake, fitness level and body composition were also assessed at each APFT. After completing the 1st APFT, subjects showed a significant increase in CK and CRP levels immediately post-exercise and in CK at 24hrs post-exercise. There was a significant decrease in GPX immediately post-exercise but no significant change in SOD following exercise. Each of the oxidative stress biomarkers were found to be influenced by the antioxidant vitamins A, C and E, fitness level, total fat mass and total fat percentage. There were also significant interactions between fitness level and vitamins A, C, and E, and between fitness level and total fat mass and total fat percentage. There was no significant effect of attempted weight loss on the exercise-induced changes in the biomarkers, but there were significant changes in BMI, fat mass and fat percentage after the weight loss period. In conclusion, the APFT produced oxidative stress in overweight subjects which was not affected by attempted weight loss. Changes in oxidative stress biomarkers at the different time points were significantly affected by dietary antioxidants, fitness level, and body composition.Item Variations in 11B-Hydroxysteroid Dehydrogenase Type1 in Two Rat Models of Obesity(2006-05-04) Parsons, Erica Zager; Castonguay, Thomas W; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Obesity is an epidemic that has been estimated to cost the United States over $117 billion every year. Glucocorticoids have long been implicated in the maintenance of energy homeostasis due to their involvement with the hypothalamic-pituitary-adrenal axis. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) is an enzyme that interconverts the glucocorticoids cortisol and cortisone, and their rat counterparts corticosterone and 11-dehydrocorticosterone. We predicted an association between hepatic levels of this enzyme and either genetic obesity or dietary-induced obesity from any of two fat levels (high fat, low fat) or three fat sources (saturated, polyunsaturated, or monounsaturated). Our results indicated that hepatic 11β-HSD-1 is downregulated in genetic obesity, as has been previously found. High fat diets also caused reductions in hepatic enzyme message, although these were not statistically significant. There did not appear to be any effect of fat type.Item THE EFFECTS OF OBESITY ON PLASMA LEVELS OF OMENTIN, A DEPOT-SPECIFIC ADIPOCYTOKINE(2004-08-27) de Souza Batista, Celia Maria; Kantor, Mark; McLenithan, John; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Obesity is a chronic pathological condition and a risk factor for diabetes and cardiovascular disease. It has been demonstrated that adipose tissue functions not only as a fat storage depot but also as an endocrine organ. Omentin is a protein expressed and secreted in adipose tissue that increases insulin-stimulated glucose transport. To further elucidate omentin's physiological function, its levels were measured by quantitative western blotting in plasma from 44 healthy nondiabetic volunteers (22 women, 22 men). Participants were organized into sibling pairs based on discordant BMI (3-12 Kg/m2). Lean subjects had significantly higher omentin levels than obese/overweight subjects (independent of sex), and significantly higher omentin levels were detected in women compared to men. Omentin levels were inversely correlated with BMI and positively correlated with HDL levels. These data suggest that omentin may play a physiological role in the pathogenesis of obesity-dependent insulin resistance.