Black R M, Conover K L, Weingarten H P
Department of Psychology, McMaster University, Hamilton, Ontario, Canada.
Am J Physiol. 1990 Sep;259(3 Pt 2):R658-61. doi: 10.1152/ajpregu.1990.259.3.R658.
This experiment evaluates the hypothesis that an accelerated rate of gastric emptying accounts for the hyperphagia and obesity after lesions of the ventromedial hypothalamus (VMH). Gastric emptying was measured for 16 days after the production of VMH lesions in rats maintained either ad libitum or on restricted eating. Only ad libitum VMH-lesioned rats demonstrated faster than normal rates of emptying. However, VMH rats maintained at control weights showed normal rates of gastric emptying and, even in ad libitum rats, accelerated emptying was not apparent immediately after lesions. These findings indicate that changes of emptying are not a primary effect of VMH lesions but that this dysfunction develops secondarily as a consequence of excess eating and weight gain. Measurement of stomach secretions demonstrated, however, that VMH lesions did result in an immediate and direct effect on gastric secretion. These findings mitigate the importance of gastric emptying in the etiology of the VMH syndrome. Other data consistent with this conclusion are reviewed.
胃排空加速是腹内侧下丘脑（VMH）损伤后食欲亢进和肥胖的原因。对自由进食或限制进食的大鼠进行VMH损伤后，连续16天测量其胃排空情况。只有自由进食的VMH损伤大鼠的胃排空速度比正常速度快。然而，体重维持在对照水平的VMH损伤大鼠的胃排空速度正常，而且即使是自由进食的大鼠，损伤后立即也未出现排空加速的情况。这些发现表明，排空变化不是VMH损伤的主要效应，而是由于过度进食和体重增加继发产生的功能障碍。然而，胃分泌的测量结果表明，VMH损伤确实对胃分泌产生了即时和直接的影响。这些发现降低了胃排空在VMH综合征病因中的重要性。本文还综述了与该结论一致的其他数据。
