satiety n : the state of being satisfactorily full and unable to take on more [syn: repletion, satiation]
- The state of being perfectly satiated.
- That loaf of bread, that jug of wine, and thou have left me in a state of utter satiety.
Cholecystokinin (CCK; from Greek chole, "bile"; cysto, "sac"; kinin, "move"; hence, move the bile-sac (gallbladder)) is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called pancreozymin, is synthesised by I-cells in the mucosal epithelium of the small intestine and secreted in the duodenum, the first segment of the small intestine, and causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively. It also acts as a hunger suppressant. Recent evidence has suggested that it also plays a major role in inducing drug tolerance to opioids like morphine and heroin, and is partly implicated in experiences of pain hypersensitivity during opioid withdrawal.
StructureCCK is composed of varying numbers of amino acids (e.g., CCK58, CCK33, CCK8) depending on post-translational modification of the CCK gene product, preprocholecystokinin. CCK is very similar in structure to gastrin, another of the gastrointestinal hormones, so much so that the last five C-terminal amino acids are the same as those of gastrin. CCK58 comprises a helix-turn-helix configuration.
Release and FunctionCCK mediates a number of physiological processes, including digestion and satiety.
DigestionSecretion of CCK by the duodenal and intestinal mucosa is stimulated by fat- or protein-rich chyme entering the duodenum. It then inhibits gastric emptying and gastric acid secretion and mediates digestion in the duodenum. It stimulates acinar cell of pancreas to produce water, ion and stimulates the secretion of a juice rich in pancreatic digestive enzymes. Together these enzymes catalyze the digestion of fat, protein, and carbohydrates. Thus the levels of the substances which stimulated the release of CCK drop and the concentration of the hormone drops as well. The release of CCK is also inhibited by somatostatin.
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 micelles that emulsify fats, aiding in their digestion and absorption.
NeurobiologyAs a neuropeptide, CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system. In humans, it has been suggested that CCK administration causes nausea and anxiety, and weakly decreases the desire to eat is the reason for CCK administration to induce a satiating effect. Some studies have given a strong correlation for the satiating effect, but have not proven or disproven that CCK administration causes nauseau or anxiety Benoit et al (2003). The mechanism for this hunger suppression is thought to be a decrease in the rate of gastric emptying.
The effects of CCK vary between individuals. For example, in rats, CCK administration significantly reduces hunger in young males, but is slightly less effective in older subjects, and even slightly less effective in females. The hunger-suppressive effects of CCK also are reduced in obese rats.
satiety in German: Cholecystokinin
satiety in Dhivehi: ކޯލިސިސްޓަކައިނިން
satiety in French: Cholécystokinine
satiety in Italian: Colecistochinina
satiety in Dutch: Cholecystokinine
satiety in Polish: Cholecystokinina
satiety in Portuguese: Colecistocinina
satiety in Serbian: Холецистокинин
satiety in Finnish: Kolekystokiniini
satiety in Swedish: Cholecystokinin