DIET EFFECT ON ENERGY METABOLISM

肥胖(ob/ob)小鼠和下丘脑肥胖大鼠 刀伤即使配对到各自的刀口也会变得肥胖 控制。因此这些动物消耗的能量必须比 很正常。我们的总体目标是确定神经内分泌和 提高饮食效率的细胞因素 这些肥胖动物体内的能量滞留。实验是 建议确定肾上腺切除术进一步阻塞的原因 喂食高淀粉食物的ob/ob小鼠肥胖的发展，但 而在喂食高糖或高脂肪食物的肥胖小鼠中则不然。的效果 这些饮食疗法通过神经控制胰岛素的分泌 离体胰岛对甲状腺的单向摄取 激素和皮质酮通过肝脏和大脑，对交感神经 心脏和棕色脂肪组织中的神经系统活动 通过棕色脂肪组织的去甲肾上腺素转换率进行评估 生热能力，以及关于 假手术动物能量平衡中的体温调节生热作用 手术和摘除肾上腺的肥胖和瘦小鼠将 已经确定了。假设中枢神经系统是 糖皮质激素的作用部位负责发展 肥胖/肥胖小鼠的肥胖，高胰岛素血症是关键 糖皮质激素诱导肥胖小鼠肥胖的介体将是 已评估。肥胖/肥胖小鼠与大鼠的选择性比较 用下丘脑刀切割将有助于确定关键因素 这使得这些动物的饮食能量保持得很高。 这些数据应该会增加我们对饮食的理解-- 肥胖发展中的依赖代谢因素，以及 应帮助确定改进的营养方法以应对 与预防和控制肥胖有关。

Obese (ob/ob) mice and rats with obesity-producing hypothalamic knife-cuts become obese even if pairfed to their respective controls. These animals must therefore expend less energy than normal. Our overall goal is to identify neuroendocrine and cellular factors responsible for the enhanced efficiency of dietary energy retention in these obese animals. Experiments are proposed to determine why adrenalectomy blocks further development of obesity in ob/ob mice fed a high-starch diet, but not in ob/ob mice fed high-glucose or high-fat diets. Effects of these dietary treatments on neural control of insulin secretion by isolated pancreatic islets, on unidirectional uptake of thyroid hormones and corticosterone by liver and brain, on sympathetic nervous system activity in heart and brown adipose tissue as assessed by norepinephrine turnover, on brown adipose tissue thermogenic capacity, and on the involvement of thermoregulatory thermogenesis in energy balance in sham- operated and adrenalectomized ob/ob and lean mice will be ascertained. The hypotheses that the central nervous system is the site of glucorticoid action responsible for development of obesity in ob/ob mice, and that hyperinsulinemia is the critical mediator of glucorticoid-induced obesity in ob/ob mice will be evaluated. Selective comparisons between ob/ob mice and rats with hypothalamic knife-cuts will help identify the key factors that permit high retention of dietary energy in these animals. These data should increase our understanding of the diet- dependent metabolic factors in development of obesity, and should aid in defining improved nutritional approaches to cope with the prevention and control of obesity.