Cholecystokinin and bombesin: peripheral signals for satiety?
1992
Gibbs, J. | Smith, G.P.
Our demonstrations that cholecystokinin (1) and bombesin (2) reduced meal size in rats initiated ongoing efforts to determine the mechanisms of action of these effects and to determine whether endogenous forms of these brain-gut peptides play physiological roles in producing satiety. Exploring these questions, studies from several laboratories have made clear progress, revealing remarkable similarities and interesting differences between cholecystokinin and bombesin. When administered peripherally, both peptides produce potent, dose-related, behaviorally specific inhibitions of short-term food intake in a variety of animal species and in humans. Whereas cholecystokinin is more potent in reducing meal size, bombesin is more potent in extending the length of the intermeal interval. The sites of action of both peptides are peripheral, not central, and their initial effects are relayed centrally by afferent nerves. Vagal section alone blocks the action of cholecystokinin, but section of both vagal and spinal visceral afferents is required to block the action of bombesin. The dorsal hindbrain, an integrative area for visceral and gustatory information, is required for the full expression of satiety for both peptides. In addition, both peptides interact with endogenous serotonin systems. Finally, the recent development of increasingly specific receptor antagonists has allowed tests of the physiological relevance of the satiety actions of endogenous cholecystokinin and bombesin-like peptides. In the case of cholecystokinin, the cumulative results provide a compelling demonstration of a critical role in controlling short-term food intake. Similar tests for bombesin are encouraging but preliminary.
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