Parkinson W L, Weingarten H P
Department of Psychology, McMaster University, Hamilton, Ontario, Canada.
Am J Physiol. 1990 Oct;259(4 Pt 2):R829-35. doi: 10.1152/ajpregu.1990.259.4.R829.
Electrolytic lesions of the ventromedial hypothalamus (VMH) produce an obesity syndrome characterized by hyperphagia, adiposity, and heightened parasympathetic tone. Experiments were conducted to evaluate the possibility that these symptoms arise from damage to distinct and separated loci within the hypothalamus. Rats received either VMH lesions, perifornical hypothalamic (PFH) knife cuts, ventromedial hypothalamic nucleus (VMN) lesions, or sham surgery (Sham). When maintained ad libitum, VMH and PFH rats were hyperphagic, overweight, and became obese. VMN rats were not hyperphagic, nor did they gain excessive weight, but they did develop an obesity reflected as a significantly elevated level of carcass fat. Under restricted feeding conditions, both VMH and VMN rats became obese; PFH rats did not. Also, only VMH lesions and PFH knife cuts increased basal gastric acid secretion. These data demonstrate dissociations between hyperphagia and obesity, as well as between stomach secretion and obesity, in the VMH syndrome. The implications of these findings for a dissociative model of the VMH obesity syndrome are discussed.
腹内侧下丘脑（VMH）的电解损伤会导致一种肥胖综合征，其特征为摄食过多、肥胖以及副交感神经张力增强。开展了实验以评估这些症状是否源于下丘脑内不同且相互分离的位点受损。给大鼠分别进行VMH损伤、穹窿周下丘脑（PFH）刀切、腹内侧下丘脑核（VMN）损伤或假手术（Sham）。当随意进食时，VMH和PFH大鼠摄食过多、超重并变得肥胖。VMN大鼠没有摄食过多，也没有体重过度增加，但它们确实出现了以显著升高的体脂水平为表现的肥胖。在限食条件下，VMH和VMN大鼠都变得肥胖；PFH大鼠没有。此外，只有VMH损伤和PFH刀切会增加基础胃酸分泌。这些数据表明，在VMH综合征中，摄食过多与肥胖之间以及胃分泌与肥胖之间存在分离。讨论了这些发现对VMH肥胖综合征解离模型的意义。
