The Role of Cholecystokinin (CCK) in Eating Behavior

Abstract

Cholecystokinin (CCK) is released from the basolateral membrane of the enteroendocrine I cell in response to the presence of nutrients, particularly fatty acids and proteins, in the intestinal lumen. Several forms of CCK are cleaved from the precursor form, with CCK-8 and CCK-58 being the most potent in suppression of food intake. Postprandial CCK stimulates pancreatic secretion, bile release, gallbladder contraction, slowing of gastric emptying and inhibition of food intake, thus controlling the passage of ingesta. Both systemic as well as brain CCK inhibit food intake. Most of CCK’s actions, including control of food intake, are mediated through CCK-1Rs acting through a paracrine mode of action on vagal afferent neurons that innervate the gastrointestinal (GI) tract and terminate in the hindbrain. Changes in dietary environment results in altered behavioral and neuronal responses to CCK. Finally, CCK interacts with several anorexigenic and orexigenic signals as well as adiposity signals to enhance their effects on meal size or energy regulation. This chapter summarizes the role of CCK as a satiation signal, its mechanisms of action, and its potential participation in the regulation of body weight.