Surwit R S, Feinglos M N, Rodin J, Sutherland A, Petro A E, Opara E C, Kuhn C M, Rebuffé-Scrive M
Department of Psychiatry, Duke University Medical Center, Durham, NC 27710, USA.
Metabolism. 1995 May;44(5):645-51. doi: 10.1016/0026-0495(95)90123-x.
We have previously demonstrated that the C57BL/6J (B/6J) 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 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/6J 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, 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 B/6J 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.
我们之前已经证明，如果将C57BL/6J（B/6J）小鼠断奶后喂食高脂肪、高蔗糖（HH）饮食，它们会出现严重肥胖、高血糖和高胰岛素血症。在本研究中，我们比较了脂肪和蔗糖单独以及联合作用对易患糖尿病和肥胖的B/6J小鼠以及抗糖尿病和肥胖的A/J小鼠的影响。4个月后，A/J小鼠的饲料效率（[FE]体重增加量除以卡路里摄入量）在不同饮食之间没有差异，但B/6J小鼠的高脂肪饲料效率显著增加。也就是说，B/6J小鼠在高脂肪饮食中体重增加更多，且摄入的卡路里并不比A/J小鼠多。饲料效率的增加与高脂肪饮食的B/6J小鼠脂肪细胞增生有关。B/6J小鼠的脂肪诱导性肥胖与肾上腺皮质活动无关。在没有脂肪的情况下，蔗糖使两种品系的饲料效率均降低。喂食低脂、高蔗糖（LH）饮食的动物实际上比喂食高复合碳水化合物饮食的动物更瘦。脂肪也是B/6J小鼠高血糖和高胰岛素血症的关键刺激因素。在没有脂肪的情况下，蔗糖对血糖或胰岛素没有影响。这些数据清楚地表明，在这两种品系的小鼠中，对脂肪代谢反应的基因差异在肥胖和糖尿病的发生发展中比高脂肪饮食增加的热量含量更为重要。
