Cholecystokinin is secreted from the same general duodenal mucosa as secretin but in response to the lipid and protein components of the meal. CCK has multiple roles that are not completely clear. The CCK molecule exists in a number of peptide chain lengths, each with differing properties but all with extreme potency. The effects of an elevation in CCK are as follows: Cholecystokinin is the main inhibitor of gastric emptying, slowing the release of nutrient-dense chyme from the stomach at a rate that is proportional to duodenal and pancreatic digestive function. CCK stimulates enzyme secretion from the pancreatic aci-nar cells and causes contraction of gallbladder wall muscle and relaxation of the sphincter of Oddi, allowing bile to flow into the duodenum.

Cholecystokinin levels directly influence levels of satiety and the perception of fullness in association with meals. Therefore, the signalling of fullness to the brain by means of CCK release is one possible pathway for the peripheral control of food intake and is of particular importance not least by virtue of the presence of CCK receptors known to be present within brain tissue. CCK secretion is inhibited by the absence of nutrients in the duodenal lumen.

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