Robeson B L, Eisen E J, Leatherwood J M
Growth. 1981 Autumn;45(3):198-215.
Polygenic obese (M16) and nonobese (ICR) mice were fed ad libitum either a high-fat (FAT) or high-carbohydrate (CHO) diet from 6 to 10 weeks of age. After this four-week period, M16 exceeded (P less than 0.01) ICR mice and FAT-fed exceeded (P less than 0.01) CHO-fed mice in body energy percent, body fat percent, and weight and proportional weight of epididymal and subcutaneous fat pads. Fat cell size and number in both fat depots were greater (P less than 0.01) in the M16 than in the ICR line. Mice fed FAT had larger (P less than 0.01) fat cells in both depots compared with CHO-fed mice, but fat cell nuber was not altered significantly. M16 mice were hyperglycemic, hyperinsulinemic and hypercholesterolemic, Dietary treatment did not affect glucose or insulin levels, but cholesterol was greater (P less than 0.01) on FAT than on CHO diet. Lipoprotein lipase and fatty acid synthetase activities were greater in M16 than in ICR mice, while fatty acid synthetase activity was greater in mice fed CHO than in those fed FAT. Genotype by diet interactions were not important for the traits studied. Polygenic obese mice, developed by selection for increased growth rate, share many of the characteristics of the single gene obesity syndromes in rodents. The development of obesity in polygenic obese mice may be due, in part, to an acceleration of the normal developmental process of growth, in addition to hyperphagia and increased energetic efficiency.
将6至10周龄的多基因肥胖（M16）小鼠和非肥胖（ICR）小鼠随意喂食高脂（FAT）或高碳水化合物（CHO）饮食。在这四周期间后，M16小鼠在身体能量百分比、体脂百分比、附睾和皮下脂肪垫的重量及相对重量方面超过（P<0.01）ICR小鼠，喂食FAT的小鼠超过（P<0.01）喂食CHO的小鼠。两个脂肪库中的脂肪细胞大小和数量在M16小鼠中均大于（P<0.01）ICR品系。与喂食CHO的小鼠相比，喂食FAT的小鼠在两个脂肪库中均具有更大（P<0.01）的脂肪细胞，但脂肪细胞数量没有显著改变。M16小鼠存在高血糖、高胰岛素血症和高胆固醇血症，饮食处理未影响血糖或胰岛素水平，但FAT饮食组的胆固醇高于（P<0.01）CHO饮食组。脂蛋白脂肪酶和脂肪酸合成酶活性在M16小鼠中高于ICR小鼠，而脂肪酸合成酶活性在喂食CHO的小鼠中高于喂食FAT的小鼠。饮食与基因型的相互作用对所研究的性状并不重要。通过选择提高生长速率培育出的多基因肥胖小鼠具有许多啮齿动物单基因肥胖综合征的特征。多基因肥胖小鼠肥胖的发生可能部分归因于正常生长发育过程的加速，此外还包括食欲亢进和能量效率提高。
