Ventromedial hypothalamic lesions elevate basal and cephalic phase gastric acid output.
With the use of a new technique for the measurement of gastric acid output in the rat, this study identifies ventromedial hypothalamic (VMH) lesion-induced changes in gastric acid secretion. Basal and cephalic phase gastric acid secretion were monitored in VMH- and sham-lesioned control rats on days 1, 5, 9, 13, and 17 postlesion as well as after the full development of obesity. VMH lesions resulted in increases of both phases of secretion. The magnitude of hypersecretion in lesioned rats developed with time and was fully developed by day 9 postlesion. The hypersecretion did not require a hyperphagia or weight gain, but its degree correlated with subsequent weight gain. These data, in conjunction with a review of VMH lesion effects on insulin secretion, suggest a widespread effect of VMH lesions on visceral secretory responses. The relevance of these data to the etiology of the VMH syndrome is discussed.
D000818:Animals; D001835:Body Weight; D004435:Eating; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism; D007031:Hypothalamus / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000209:etiology; D051381:Rats