Yang M U, Presta E, Björntorp P
Obesity Research Center, St Luke's-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, NY 10025.
Am J Clin Nutr. 1990 Jun;51(6):970-8. doi: 10.1093/ajcn/51.6.970.
Rats with diet-induced obesity starved for 8, 15, and 25 d lost liver and muscle glycogen, excess protein, and fat in proportion to duration of starvation. Fat-cell size decreased but fat-cell number did not. Upon refeeding, body fat was only partly restored, with further increase in adipocyte hyperplasia occurring in the starved obese rats. In contrast, fat-cell size was restored to near that of the prefasting value in the starved controls (dry-food-fed, fasted 4 d) after refeeding. With refeeding, food efficiency increased only if starvation had caused a reduction of adipocyte size below normal. Change in food efficiency was not associated with decreases in total carcass protein, specific tissue proteins, or glycogen stores but was correlated with degree of adipocyte filling. It is possible that adipose tissue status somehow modulates energy-dissipating mechanisms.
饮食诱导肥胖的大鼠禁食8天、15天和25天后，肝脏和肌肉糖原、多余蛋白质以及脂肪的减少与禁食持续时间成比例。脂肪细胞大小减小，但脂肪细胞数量未变。重新喂食后，饥饿的肥胖大鼠体内脂肪仅部分恢复，同时脂肪细胞增生进一步增加。相比之下，饥饿的对照组大鼠（喂食干粮，禁食4天）重新喂食后，脂肪细胞大小恢复至接近禁食前的水平。重新喂食时，只有当饥饿导致脂肪细胞大小降至正常水平以下时，食物效率才会提高。食物效率的变化与胴体总蛋白、特定组织蛋白或糖原储备的减少无关，但与脂肪细胞充盈程度相关。脂肪组织状态可能以某种方式调节能量消耗机制。
