CCK

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Cholecystokinin is a polypeptide hormone composed of 33 amino acids. All biological activity is in the c-terminal octapeptide fragment. It was originally extracted from the upper intestines of animals, and later found to be present in the cerebral cortex, hippocampus, amygdala, and hypothalamus. Its peripheral effects have been relatively clear. It can stimulate the stomach to secrete gastric acid, the liver to secrete bile, inhibit the absorption of sodium and water in the ileum, and stimulate the islets to release insulin and glucagon. The central role is not very clear. Some data show that it is related to feeding behavior and also related to obesity. It is also involved in pain regulation.

Introductions

Cholecystokinin (CCK, PZ) was proven and purified in 1928 and 1943. There are many natural CCK chemical structures, including CCK-33, CCK-39, CCK-58, and an 8-peptide CCK isolated from goat and human cerebellum. CCK-containing cells exist in mammalian duodenum and jejunum mucosa, and their cells are the same as human intestinal I cell. In 1978, it was discovered that CCK also exists in the central nervous system, and its content is greater than that in the small intestine. It exists in the frontal cortex, cortical piriform area, caudate nucleus, hippocampus, thalamus, hypothalamus, cerebellum, and diencephalon. CCK degrades quickly in the blood, and its half-life is about 3 minutes. It has a variety of biological effects, mainly to stimulate the secretion and synthesis of pancreatic enzymes, enhance the secretion of pancreatic bicarbonate, stimulate the contraction of the gallbladder and the relaxation of Oddi’s sphincter, it can also excite the secretion of liver and bile, regulate the movement of the small intestine and colon, and can also be used as a feeling of satiety Factors regulate food intake.

Functions

The main role of cholecystokinin is to promote the secretion of various digestive enzymes in the pancreatic acinar, to promote the contraction of the gallbladder, and to discharge bile. It has a weaker secretory effect on water and HCO3-. CCK can also act on the afferent fibers of the vagus nerve and stimulate the secretion of pancreatic enzymes through the vagus-vagus reflex. CCK activates the phosphatidyl alcohol system and acts on the pancreas under the mediation of Ca²⁺. CCK and secretin have a synergistic effect. After eating, the protein hydrolysate can stimulate the small intestinal mucosa to release a cholecystokinin-releasing peptide and stimulate the secretion of CCK by the small intestinal mucosa I cells. The factors that cause CCK secretion are from strong to weak: protein breakdown products, fatty acid salts, HCl, fat, and sugar have no effect. In addition, insulin can enhance the amylase secretion effect of cholecystokinin. The secretion of Cholecystokinin-releasing peptide in the small intestinal mucosa is very sensitive to trypsin. Trypsin can inactivate CCK release peptide. Therefore, after CCK release peptide causes CCK release and increase in pancreatin secretion, trypsin will inactivate it again, thus giving feedback Sexually inhibits the further secretion of CCK and pancreatin. The physiological significance of feedback regulation of pancreatin secretion is to prevent excessive secretion of pancreatin.

Principle

Through the complex action of special food and various enzymes in the body, it helps to decompose protein decomposition products, fatty acid salts, HCl and other decomposition factors that stimulate CCK (cholecystokinin) secretion, stimulate the inner hypothalamus, and generate a large amount of satiety signals. CCK is easily degraded in the blood to lose its activity, and its half-life is about 3 minutes. At this time, it is necessary to inhibit the secretion of trypsin, and continuously decompose the CCK decomposition factor to stimulate the secretion of CCK, so that the satiety signal continues to stimulate the hypothalamus. It also acts on the nerves of the Feeding Center to inhibit appetite production.

Interactions

It has been shown that CCK interacts with cholecystokinin A receptors mainly located on pancreatic acinar cells, and interacts with cholecystokinin B receptors mainly in the brain and stomach. The CCKB receptor also binds to gastrin, a gastrointestinal hormone that stimulates gastric acid release and gastric mucosal growth. CCK has also been shown to interact with pancreatic calcineurin. Calcineurin will continue to activate the transcription factor NFAT 1-3, which will stimulate pancreatic hypertrophy and growth. High-protein diet or protease inhibitors can stimulate CCK. CCK has been shown to interact with orexin neurons to control appetite and wakefulness (sleep). CCK can indirectly affect sleep regulation.

Figure 2. Effects of cholecystokinin on the gastrointestinal tract.

Reference

1. Kapas L.; et al. Metabolic signals in sleep regulation: the role of cholecystokinin. The Journal of Neuroscience (PhD thesis). University of Szeged. 2010