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dc.contributor.authorHaring, Samantha Jean
dc.date.accessioned2014-03-04T18:24:29Z
dc.date.available2014-03-04T18:24:29Z
dc.date.issued2009-12
dc.identifier.otherharing_samantha_j_200912_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/haring_samantha_j_200912_ms
dc.identifier.urihttp://hdl.handle.net/10724/26064
dc.description.abstractTo determine whether leptin resistance caused by a high fructose diet is due to fructose specifically or to increased dietary monosaccharide, we tested leptin responsiveness in rats fed 30% kcal fat diets containing 50% kcal glucose, 40% kcal fructose, or 15% kcal fructose. Intraperitoneal injections of 2.0 mg leptin/kg inhibited 14 hour weight gain and food intake in rats fed 40% fructose or glucose diet for 9 weeks, but not in those fed the 15% fructose diet. Leptin stimulated phosphorylation of signal transducer and activator of transcription 3 (PSTAT-3) in the medial and central nucleus of solitary tract in 40% fructose-fed animals, but not in the hypothalamic arcuate nucleus of any group. In a second study only glucose-fed animals responded to central leptin infusions although all animals remained insulin sensitive. Therefore, dietary monosaccharides may act at sites other than the hypothalamus to reverse high-fat diet induced leptin resistance.
dc.languageeng
dc.publisheruga
dc.rightspublic
dc.subjectleptin
dc.subjectfructose
dc.subjectSTAT-3, immunohistochemistry
dc.subjectarcuate nucleus
dc.subjectnucleus of the solitary tract
dc.subjectleptin resistance
dc.titleDietary carbohydrate interacts with dietary fat to influence leptin responsiveness in rats
dc.typeThesis
dc.description.degreeMS
dc.description.departmentFoods and Nutrition
dc.description.majorFoods and Nutrition
dc.description.advisorRuth Harris
dc.description.committeeRuth Harris


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