The role of CCK-like peptides in appetite regulation.
The physiological dose levels for the classically defined functions of CCK peptides, i.e., their effect on gall bladder contraction and release of pancreatic enzymes, are well established. However, the reported effects of peripheral administration of these peptides on regulation of satiety are achieved only at levels greatly in excess of the physiological range achieved in response to feeding. Thus, endogenous peripheral CCK alone would appear not to be the physiological satiety factor. The observations by Della-Fera et al. (1981) that lateral ventricular infusion into sheep of antibody to CCK results in increased feeding, if confirmed by other investigators and in other species, is the strongest evidence for a CSF-mediated role for CCK peptides in the regulation of satiety. However, numerous reports now delineate a variety of other CNS functions for these peptides. With so many effects reported, it is difficult at present to be certain which are real, which are direct or acting indirectly through another system, or which are the physiologically important functions. It can be expected that another decade will be required to sort out and define fully the multiple roles of CCK peptides that are synthesized independently in mucosal and in neuronal tissues.
D000818:Animals; D001069:Appetite Regulation / Q000187:drug effects; D001921:Brain / Q000502:physiology*; D001923:Brain Chemistry; D002766:Cholecystokinin / Q000032:analysis / Q000494:pharmacology / Q000502:physiology*; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D011956:Receptors, Cell Surface / Q000502:physiology; D011949:Receptors, Cholecystokinin; D012528:Satiety Response / Q000187:drug effects; D013552:Swine
D011956:Receptors, Cell Surface; D011949:Receptors, Cholecystokinin; D002766:Cholecystokinin