Cholecystokinin: Difference between revisions
imported>Gareth Leng (New page: '''Cholecystokinin''' (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the duodenum, and secreted in response to the presence of partially digested [[li...) |
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'''Cholecystokinin''' (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the [[duodenum]], and secreted in response to the presence of partially digested [[lipid]]s and [[protein]]s. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the [[pancreas]] and [[bile]] from the [[gall bladder]] by acting at CCK-1 receptors (formerly known as CCK-A receptors, these are mainly found in the periphery, including on vagal afferent nerve endings but are also found in some areas of the CNS). Because gastric emptying is inhibited, the partially digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines. | '''Cholecystokinin''' (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the [[duodenum]], and secreted in response to the presence of partially digested [[lipid]]s and [[protein]]s. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the [[pancreas]] and [[bile]] from the [[gall bladder]] by acting at CCK-1 receptors (formerly known as CCK-A receptors, these are mainly found in the periphery, including on vagal afferent nerve endings but are also found in some areas of the CNS). Because gastric emptying is inhibited, the partially digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines. | ||
Revision as of 09:25, 11 October 2010
Cholecystokinin (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the duodenum, and secreted in response to the presence of partially digested lipids and proteins. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at CCK-1 receptors (formerly known as CCK-A receptors, these are mainly found in the periphery, including on vagal afferent nerve endings but are also found in some areas of the CNS). Because gastric emptying is inhibited, the partially digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines.
CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting), CCK stimulates the expression of receptors associated with the stimulation of food intake, including receptors for melanin concentrating hormone (MCH)-1 and [[cannabinoid] CB1 receptors. At high levels (after food consumption), MCH-1 and CB1 receptors are down-regulated. Therefore CCK present at a high or low concentration can affect how afferent vagal neurons respond to other neurohormones.
In rats, CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females.