Cholecystokinin and satiety: current perspectives.
In the almost 30 years since the ability of peripheral administration of the brain/gut peptide cholecystokinin (CCK) to inhibit food intake was first demonstrated, significant progress in our overall understanding of the role of CCK in ingestive behavior has been made. A physiologic role for endogenous CCK in the control of meal size has been demonstrated and sites and mechanisms of action for CCK in food intake have been investigated. Recent work has uncovered roles for the CCK satiety pathway in the mediation of the feeding modulatory actions of estradiol, insulin, and leptin. The availability of the Otsuka Long Evans Tokushima Fatty (OLETF) rat, a strain lacking CCK(A) receptors, provides a unique model for the study of how deficits in a within-meals satiety signaling pathway may result in long-term changes in food intake and body weight.
Moran
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Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. tmoran@jhmi.edu
D000818:Animals; D001069:Appetite Regulation / Q000187:drug effects / Q000502:physiology*; D002766:Cholecystokinin / Q000494:pharmacology / Q000502:physiology*; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D004734:Energy Metabolism / Q000187:drug effects; D006801:Humans; D006963:Hyperphagia / Q000503:physiopathology; D023421:Models, Animal; D009765:Obesity / Q000503:physiopathology*; D051381:Rats; D020334:Rats, Inbred OLETF; D011949:Receptors, Cholecystokinin / Q000172:deficiency / Q000502:physiology*; D012527:Satiation / Q000187:drug effects* / Q000502:physiology
D011949:Receptors, Cholecystokinin; D002766:Cholecystokinin