CHOLECYSTOKININ AND CONTROL OF FOOD-INTAKE

Two mechanisms have been suggested for the inhibitory effect of cholec ystokinin on food intake: a central action of brain cholecystokinin on the brain feeding system, and a peripheral, presumably hormonal, acti on of gut cholecystokinin mediated by abdominal vagal afferent nerves. Existing evidence suggests that 1) endogenous cholecystokinin contrib utes to the production of satiety, 2) this satiety effect is primarily mediated by the type A receptor subtype, which is predominantly locat ed in the periphery, but also found in discrete regions of the central nervous system, 3) postprandial increases in circulating cholecystoki nin 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 an d (or) peripherally by endocrine, paracrine, or neurocrine mechanisms to produce satiety. Peripheral actions of cholecystokinin that may con tribute directly or indirectly to the production of satiety include in hibition of gastric emptying, activation of visceral sensory nerves, s timulation of the exocrine pancreas and gallbladder to facilitate dige stion and absorption of ingested nutrients, and stimulation of insulin secretion.