<P> Once in the circulatory system, CCK has a relatively short half - life . </P> <P> CCK mediates digestion in the small intestine by inhibiting gastric emptying . It stimulates the acinar cells of the pancreas to release a juice rich in pancreatic digestive enzymes (hence an alternate name, pancreozymin) that catalyze the digestion of fat, protein, and carbohydrates . Thus, as the levels of the substances that stimulated the release of CCK drop, the concentration of the hormone drops as well . The release of CCK is also inhibited by somatostatin and pancreatic peptide . Trypsin, a protease released by pancreatic acinar cells, hydrolyzes CCK - releasing peptide and monitor peptide, in effect turning off the additional signals to secrete CCK . </P> <P> CCK also causes the increased production of hepatic bile, and stimulates the contraction of the gall bladder and the relaxation of the sphincter of Oddi (Glisson's sphincter), resulting in the delivery of bile into the duodenal part of the small intestine . Bile salts form amphipathic lipids, micelles that emulsify fats, aiding in their digestion and absorption . </P> <P> As a peptide hormone, CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system . The mechanism for hunger suppression is thought to be a decrease in the rate of gastric emptying . CCK also has stimulatory effects on the vagus nerve, effects that can be inhibited by capsaicin . The stimulatory effects of CCK oppose those of ghrelin, which has been shown to inhibit the vagus nerve . </P>

The presence of fat in the intestines stimulates cells