Turkenkopf I J, Maggio C A, Greenwood M R
J Nutr. 1982 Jul;112(7):1254-63. doi: 10.1093/jn/112.7.1254.
Zucker rats were early weaned onto either medium-chain (MCT) or long-chain triglycerides (LCT) to examine the effect on the development of obesity. Preobese and lean pups were weaned at 16 days to isocaloric, isonitrogenous liquid diets containing either 65% MCT or LCT (by calories) or to a "stocklike" (5.5% fat, 72.6% carbohydrate) control diet or were pair-fed stocklike diet to MCT-fed rats until day 45. MCT-feeding lowered body weight gain and fat pad weight in obese and lean rats compared to stocklike-fed controls. Additionally, fat cell size and lipoprotein lipase (LPL) activity and hepatic acetyl CoA carboxylase activity were reduced in obese MCT-fed rats compared to obese controls fed stocklike diet. Except for altered LPL activity the effects produced by MCT-feeding were attributable to its anorectic effect. However, all obese rats, including the MCT group, developed an obese body composition and were hyperinsulinemic. The development sequence leading to obesity may be derived from a fundamental cellular defect that results in metabolic alterations in different tissues at critical periods of development. Thus, effective treatment of this genetic obesity requires a better understanding of fa gene action.
将 Zucker 大鼠在早期断奶后分别给予中链甘油三酯（MCT）或长链甘油三酯（LCT），以研究其对肥胖症发展的影响。将肥胖前期和瘦的幼鼠在 16 日龄时断奶，给予等热量、等氮的液体饮食，其中含有 65%的 MCT 或 LCT（按热量计算），或给予“类常规”（5.5%脂肪，72.6%碳水化合物）对照饮食，或将类常规饮食成对喂给 MCT 喂养的大鼠，直至第 45 天。与类常规饮食喂养的对照组相比，MCT 喂养降低了肥胖和瘦大鼠的体重增加以及脂肪垫重量。此外，与类常规饮食喂养的肥胖对照组相比，MCT 喂养的肥胖大鼠的脂肪细胞大小、脂蛋白脂肪酶（LPL）活性和肝脏乙酰辅酶 A 羧化酶活性均降低。除了 LPL 活性改变外，MCT 喂养产生的影响归因于其厌食作用。然而，所有肥胖大鼠，包括 MCT 组，均形成了肥胖的身体组成且胰岛素血症升高。导致肥胖的发育序列可能源于一种基本的细胞缺陷，这种缺陷在发育的关键时期导致不同组织的代谢改变。因此，有效治疗这种遗传性肥胖需要更好地了解 fa 基因的作用。
