CHOLECYSTOKININ AND CONTROL OF FOOD-INTAKE

Two mechanisms have been suggested for the inhibitory effect of cholecystokinin on food intake: a central action of brain cholecystokinin on the brain feeding system, and a peripheral, presumably hormonal, action of gut cholecystokinin mediated by abdominal vagal afferent nerves. Existing evidence suggests that 1) endogenous cholecystokinin contributes to the production of satiety, 2) this satiety effect is primarily mediated by the type A receptor subtype, which is predominantly located in the periphery, but also found in discrete regions of the central nervous system, 3) postprandial increases in circulating cholecystokinin are neither sufficient nor necessary for normal satiety to occur, and 4) activation of abdominal vagal afferent neurons is not the only means by which endogenous cholecystokinin produces satiety. It remains to be determined whether endogenous cholecystokinin acts centrally and (or) peripherally by endocrine, paracrine, or neurocrine mechanisms to produce satiety. Peripheral actions of cholecystokinin that may contribute directly or indirectly to the production of satiety include inhibition of gastric emptying, activation of visceral sensory nerves, stimulation of the exocrine pancreas and gallbladder to facilitate digestion and absorption of ingested nutrients, and stimulation of insulin secretion.