Abstract
Gastric distention was produced through a water-filled-balloon system and the electrical activity of the hypothalamic "satiety" and "feeding" centers were recorded electroencephalographically through stereotaxically implanted electrodes. Gastric distention leads to production of high voltage irregular waves and occasional spikes, selectively in the region of the satiety centers. Gastric hunger contractions do not change the electrical activity of either feeding or satiety centers. Glucagon does not produce any direct effect on the hypothalamic centers or stomach contractions. Later, when glucagon raises blood glucose and arteriovenous Δ-glucose, activity of satiety centers increases and gastric contractions are inhibited. After lesions of satiety centers, rise in blood glucose with glucagon does not inhibit gastric contractions. Therefore, the inhibition of gastric hunger contractions is a result of activation of satiety centers by increased glucose utilization.
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