Alterations in gastric secretion following hypothalamic lesions producing hyperphagia

Abstract

Fasting gastric secretion and secretion during insulin hypoglycemia were collected from hypothalamic hyperphagic rats equipped with chronic gastric fistula in an attempt to correlate the hypothalamic neural mechanisms controlling food intake with gastric secretion. The interdigestive or basal fasting secretion of rats rendered hyperphagic by stereotaxic ablation of the ventromedial nuclei was significantly increased in volume, acid concentration and output, and pepsin output when compared with control and sham-operated rats and rats with hypothalamic lesions without hyperphagia. Hypothalamic hyperphagic rats did not show a significant increase in gastric secretion during insulin hypoglycemia, whereas the other groups did. The levels of hypoglycemia induced by insulin were comparable in all groups. These studies suggest an important role of the ventromedial nuclei in the central regulation of acid and pepsin secretion, and also relate the hypothalamic neural control of gastric secretion to that of food intake. The results also indicate that this nucleus is involved either as a "center" or pathway in the augmentation of gastric secretion by insulin hypoglycemia.