Elsevier

Metabolism

Volume 44, Issue 5, May 1995, Pages 645-651
Metabolism

Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and AJ mice

https://doi.org/10.1016/0026-0495(95)90123-XGet rights and content
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Abstract

We have previously demonstrated that the C57BL/6J (B6J) 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 B6J and diabetes- and obesity-resistant AJ mice. After 4 months, the feed efficiency ([FE] weight gained divided by calories consumed) did not differ across diets in AJ mice, but B6J mice showed a significantly increased FE for fat. That is, B6J mice gained more weight on high-fat diets without consuming more calories than AJ mice. The increase in FE was related to adipocyte hyperplasia in B6J mice on high-fat diets. Fat-induced obesity in B6J 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 B6J 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.

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Supported by the John D. and Catherine T. MacArthur Foundation Research Program on the Determinants and Consequences of Health Promoting and Health Damaging Behavior, National Institutes of Health Grant No. R01 (DK24923), a grant from the American Diabetes Association, and a National Institute of Mental Health Research Scientist Award (MH00303).