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Science 29 September 1989:
Vol. 245. no. 4925, pp. 1509 - 1511
DOI: 10.1126/science.2781294
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Articles

Science, Vol 245, Issue 4925, 1509-1511
Copyright © 1989 by American Association for the Advancement of Science

articles

Postponement of satiety by blockade of brain cholecystokinin (CCK-B) receptors

CT Dourish, W Rycroft, and SD Iversen

Merck Sharp & Dohme Research Laboratories, Neuroscience Research Center, Terlings Park, Harlow, Essex, England.

Exogenous cholecystokinin (CCK) decreases food intake and causes satiety in animals and man. However, it has not been established that endogenous CCK causes satiety or whether the response is mediated by peripheral-type (CCK-A) or brain-type (CCK-B) receptors. The development of potent and selective antagonists for CCK-A (MK-329) and CCK-B (L-365,260) receptors now allows these issues to be addressed. The CCK-A antagonist MK-329 and the CCK-B antagonist L-365,260 increased food intake in partially satiated rats and postponed the onset of satiety; however, L-365,260 was 100 times more potent than MK-329 in increasing feeding and preventing satiety. These results suggest that endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain.


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