Walgren M C, Powley T L
Am J Physiol. 1985 Feb;248(2 Pt 2):R172-80. doi: 10.1152/ajpregu.1985.248.2.R172.
The present study was undertaken to determine the relative contributions of altered metabolic responses and excess food intake to the obesity and hyperinsulinemia of the ventromedial hypothalamic (VMH) syndrome. This experiment, employing an intragastric hyperalimentation protocol, was also designed to address the related issue of whether altered energy utilization serves as a compensatory strategy for reducing energy retention in the face of excess intake. Separate groups of VMH-lesioned and sham-lesioned female rats were fed, either orally or intragastrically, up to 200% of the calories ingested by a normally feeding intact rat. Both VMH-lesioned and intact rats became obese and hyperinsulinemic when hyperalimented for 30 days, but rats with lesions deposited 25% more fat than intact animals receiving an identical number of calories. Estimates of total carcass energy indicated that rats with lesions required 11% less calories than intact rats to retain identical levels of energy. Furthermore, intact hyperalimented rats failed to evidence the caloric wastage that has been reported to occur in orally fed rats that overeat cafeteria diets.
本研究旨在确定代谢反应改变和食物摄入过量对腹内侧下丘脑(VMH)综合征所致肥胖和高胰岛素血症的相对影响。本实验采用胃内高营养方案,还旨在解决一个相关问题,即能量利用改变是否作为一种补偿策略,在摄入过量时减少能量潴留。将VMH损伤的雌性大鼠和假手术损伤的雌性大鼠分为不同组,通过口服或胃内给予高达正常进食的完整大鼠摄入热量200%的食物。VMH损伤的大鼠和完整大鼠在高营养喂养30天后均出现肥胖和高胰岛素血症,但损伤大鼠比摄入相同热量的完整动物多沉积25%的脂肪。对整个胴体能量的估计表明,损伤大鼠比完整大鼠在保留相同能量水平时所需热量少11%。此外,高营养喂养的完整大鼠未表现出据报道在自由选择进食自助餐饮食的大鼠中出现的热量浪费。