NAASO Meeting 2005, Vancouver #5
A New Rat Model of Dietary Obesity and Hypertension.
J.L. Johnson, D.P. Wan, R.J. Koletsky & Paul Ernsberger Department of Nutrition, Case Western Reserve University, Cleveland, Oh 44106
Induction of dietary obesity in the spontaneously hypertensive rat (SHR) strain would facilitate study of the interactions between obesity and hypertension. Mutant rats on the same genetic background have a nonsense mutation of the leptin receptor (SHROB) and become extremely obese on normal chow. Several other groups have fed solid diets high in fat and sugar to SHR and failed to induce weight gain, implying resistance to dietary obesity. We developed a liquid dietary supplement providing 32% sucrose + 8% heavy whipping cream +micronutrients. After 70d a 25% weight gain was achieved while controls gained less than 5%. The depot most expanded in males was the retroperitoneal (♂: 250%, ♀: 150%) and in females the gonadal (♂: 81%, ♀: 250%) while mesenteric fat increased for both genders (♂: 245%, ♀: 237%). Genetic obesity most affected the subscapular depot in both genders. Dietary obese SHR showed even higher blood pressures (227±7mmHg; N=8) than control SHR (199±8; N=8) and also higher pressures than genetically obese SHROB (190±2; N=18). Cardiac hypertrophy was present in both dietary and genetic obesities. Fasting insulin was increased in dietary obese SHR (1.35±0.07ng/ml) compared to control SHR (0.46±0.05) but were below levels in SHROB (5.0±2.2). In an oral glucose tolerance test, the glucose area under the curve showed a similar pattern of differences (dietary obese SHR: 18.5 g*min/dL control SHR: 8.07; SHROB: 24.8). Thus, comparison of dietary and genetic obesities on the SHR background will allow inferences about the role of leptin in metabolism and blood pressure regulation.
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