Accelerated gastric emptying in VMH-lesioned rats is secondary to excess weight gain.

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.