Publication Date:
1989-09-29
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dourish, C T -- Rycroft, W -- Iversen, S D -- New York, N.Y. -- Science. 1989 Sep 29;245(4925):1509-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Sharp & Dohme Research Laboratories, Neuroscience Research Center, Terlings Park, Harlow, Essex, England.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2781294" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Benzodiazepines/pharmacology
;
Benzodiazepinones/pharmacology
;
Brain/drug effects/*physiology
;
Cholecystokinin/antagonists & inhibitors/*physiology
;
Devazepide
;
Male
;
*Phenylurea Compounds
;
Rats
;
Rats, Inbred Strains
;
Receptors, Cholecystokinin/drug effects/*physiology
;
Satiation/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
