Dulloo A G, Girardier L
Department of Physiology, University of Geneva, Switzerland.
Am J Physiol. 1989 Oct;257(4 Pt 2):R717-25. doi: 10.1152/ajpregu.1989.257.4.R717.
The influence of experimental hyperinsulinemia on energy intake, energy expenditure, and body composition was investigated in rats treated chronically with high doses of insulin. Energy balance studies, each of 2-wk duration, were conducted with two different long-acting insulins (Protamine and Monotard), administered in the morning (IM), the late afternoon (IA), or both (IMA) and in animals of three different ages, namely in 4-, 8-, and 12-wk-old rats. The results indicate that the level of hyperphagia induced by insulin was markedly influenced by the type of long-acting insulin (P less than 0.001; Protamine greater than Monotard), by age (P less than 0.001; 12 greater than 8 greater than 4 wk), as well as by the timing of insulin administration (P less than 0.002, IMA greater than IM or IA). Body protein deposition was unaltered, but body fat and energy expenditure increased in parallel to the level of hyperphagia. Regression analysis shows a strong linear correlation (r = 0.963) between the change in energy expenditure and the change in energy intake in response to insulin and indicates that approximately 50% of the excess calories consumed was dissipated as heat. In the absence of hyperphagia, however, insulin administration had no effect on energy expenditure nor on energy partitioning. Similarly, the influence of altered meal pattern, induced by administering insulin at different times of the day, was also found to have no impact on energy expenditure. The current investigations therefore refute the notion that high doses of insulin via hyperinsulinemia and/or altered meal pattern have an inhibitory influence on whole body thermogenesis. In contrast, our data demonstrate that the adaptive phenomenon that tends to minimize the accumulation of excess caloric intake, i.e., diet-induced thermogenesis, persists in the hyperinsulinemic state.
在长期接受高剂量胰岛素治疗的大鼠中，研究了实验性高胰岛素血症对能量摄入、能量消耗和身体组成的影响。使用两种不同的长效胰岛素（鱼精蛋白胰岛素和单组分胰岛素）进行了为期2周的能量平衡研究，分别在上午（IM）、下午晚些时候（IA）或两者同时（IMA）给药，并在三种不同年龄的动物中进行，即4周龄、8周龄和12周龄的大鼠。结果表明，胰岛素诱导的摄食过量水平受到长效胰岛素类型（P<0.001；鱼精蛋白胰岛素大于单组分胰岛素）、年龄（P<0.001；12周龄大于8周龄大于4周龄）以及胰岛素给药时间（P<0.002，IMA大于IM或IA）的显著影响。身体蛋白质沉积未改变，但身体脂肪和能量消耗与摄食过量水平平行增加。回归分析显示，能量消耗的变化与胰岛素刺激后能量摄入的变化之间存在强线性相关性（r = 0.963），表明摄入的多余热量中约50%以热量形式消散。然而，在没有摄食过量的情况下，注射胰岛素对能量消耗和能量分配没有影响。同样，在一天不同时间注射胰岛素所导致的进食模式改变，对能量消耗也没有影响。因此，目前的研究反驳了高剂量胰岛素通过高胰岛素血症和/或改变进食模式对全身产热有抑制作用的观点。相反，我们的数据表明，在高胰岛素血症状态下，倾向于最小化多余热量摄入积累的适应性现象，即饮食诱导产热，仍然存在。
