DIFFERENTIAL-EFFECTS OF FAT AND SUCROSE ON THE DEVELOPMENT OF OBESITYAND DIABETES IN C57BL 6J AND A/J MICE/

We have previously demonstrated that the C57BL/6J (B/6J) mouse will de velop severe obesity, hyperglycemia, and hyperinsulinemia if weaned on to a high-fat, high-sucrose (HH) diet. In the present study, we compar ed the effects of fat and sucrose separately and in combination on dia betes- and obesity-prone B/6J and diabetes- and obesity-resistant A/J mice. After 4 months, the feed efficiency ([FE] weight gained divided by calories consumed) did not differ across diets in A/J mice, but B/6 J mice showed a significantly increased FE for fat. That is, B/6J mice gained more weight on high-fat diets without consuming more calories than A/J mice, The increase in FE was related to adipocyte hyperplasia in B/6J mice on high-fat diets. Fat-induced obesity in B/6J 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, hi gh-sucrose (LH) diet were actually leaner than animals fed a high-comp lex-carbohydrate diet. Fat was also found to be the critical stimulus for hyperglycemia and hyperinsulinemia in B/6J mice. In the absence of fat, sucrose had no effect on plasma glucose or insulin. These data c learly show that across these two strains of mice, genetic differences in the metabolic response to fat are more important in the developmen t of obesity and diabetes than the increased caloric content of a high -fat diet. Copyright (C) 1995 by W.B. Saunders Company