Vilberg T R, Keesey R E
Am J Physiol. 1984 Jul;247(1 Pt 2):R183-8. doi: 10.1152/ajpregu.1984.247.1.R183.
Activity, O2 consumption, and body composition were measured in female rats with lesions of the ventromedial hypothalamus (VMH). One group of lesioned rats was food restricted to maintain body weights at control levels. O2 consumption of these food-restricted VMH-lesioned rats was 13% lower than that of nonlesioned rats. About half this energy savings accrued from reduced activity; the remainder resulted from a decline in resting metabolic rate (RMR). Though matched in weight to controls, the body composition of the restricted VMH-lesioned rats was abnormal. Their carcass protein was reduced by 12%, whereas fat was elevated 200%. The replacement of lean metabolically active tissue by carcass fat appears to underlie the reduction in RMR, an interpretation supported by multiple-regression analysis of carcass composition. Ad libitum-fed VMH-lesioned rats did not show this carcass protein decline, though their fat was elevated 895%. These results confirm that reduced activity contributes to energy savings and weight gain after VMH lesions. Likewise, restricting weight of VMH-lesioned rats to control levels reduced RMR, apparently because carcass protein declines. But, since ad libitum-fed female VMH-lesioned rats do not display reduced carcass protein, the historic assumption that RMR reductions contribute to their obesity appears unwarranted.
对患有腹内侧下丘脑(VMH)损伤的雌性大鼠的活动量、耗氧量和身体组成进行了测量。一组VMH损伤的大鼠进行食物限制,以将体重维持在对照水平。这些食物限制的VMH损伤大鼠的耗氧量比未损伤大鼠低13%。约一半的能量节省来自活动量减少;其余则是由于静息代谢率(RMR)下降。尽管体重与对照组匹配,但食物限制的VMH损伤大鼠的身体组成是异常的。它们的胴体蛋白减少了12%,而脂肪增加了200%。胴体脂肪取代了代谢活跃的瘦组织似乎是RMR降低的原因,这一解释得到了胴体组成多元回归分析的支持。自由进食的VMH损伤大鼠虽然脂肪增加了895%,但并未出现胴体蛋白下降。这些结果证实,活动量减少有助于VMH损伤后节省能量和体重增加。同样,将VMH损伤大鼠的体重限制在对照水平会降低RMR,显然是因为胴体蛋白下降。但是,由于自由进食的雌性VMH损伤大鼠并未表现出胴体蛋白减少,因此,认为RMR降低导致其肥胖的传统假设似乎没有根据。