Cholecystokinin

Purpose of review The hormone cholecystokinin was discovered in 1928 because of its ability to induce gallbladder contraction. Since then, cholecystokinin has been shown to possess multiple functions in the gastrointestinal tract and brain. This review discusses several significant developments in cholecystokinin biology that show how it plays a role in gastrointestinal diseases, including control of appetite. Recent findings Cholecystokinin was shown to induce satiety by interacting through CCK-1 receptors located in specialized regions of the hindbrain. Cholecystokinin also inhibits expression of orexigenic peptides in the hypothalamus and prevents stimulation of specialized neurons by ghrelin. In the pancreas, cholecystokinin increased the proliferation of insulin-producing beta cells and reduced insulin-induced hyperphagia. Elevated cholecystokinin levels decreased appetite and reduced intestinal inflammation caused by parasites and bacterial toxins. Summary Understanding the mechanisms by which cholecystokinin regulates orexigenic pathways in the body may lead to strategies for controlling appetite-related disorders such as obesity and bulimia. The reduction of intestinal inflammation by dietary fats (by elevating cholecystokinin) suggests that the hormone plays an integrated role in regulating the ingestion and digestion of food that may be relevant to inflammatory diseases of the gastrointestinal tract.