Theses and Dissertations from UMD

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New submissions to the thesis/dissertation collections are added automatically as they are received from the Graduate School. Currently, the Graduate School deposits all theses and dissertations from a given semester after the official graduation date. This means that there may be up to a 4 month delay in the appearance of a give thesis/dissertation in DRUM

More information is available at Theses and Dissertations at University of Maryland Libraries.

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    The Impacts of Branched Chain Amino Acid Supplementation on Adipocyte Function
    (2021) Gregory, Tabitha; Sunny, Nishanth E; Animal Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    The branched chain amino acids (BCAAs) are three essential amino acids: valine, leucine, and isoleucine. Adipose tissue has high rates of BCAA degradation and this has been shown to fuel normal function. Recent literature highlights cross- talk between BCAAs, lipid metabolism, and mitochondrial dysfunction. The objective of this thesis is to determine the impact of BCAA supplementation on adipose development, morphology, and various aspects of energy metabolism including BCAA degradation and lipolysis.C57-BL6N mice were reared on either low-fat (LF), LF with 150% BCAAs (LB), high-fat (HF), or HF with 150% BCAAs (HB) diets for 12-34 weeks. Adipose tissue morphology and energetics were determined. Results demonstrated that BCAA supplementation reduced lipid storage in visceral adipose depots, lowered circulating leptin, and reduced lipid accumulation in brown adipose tissue. BCAA supplementation also induced lipolysis, which raised circulating fatty acids. These results could have implications in the treatment and prevention of metabolic diseases.
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    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.