Everything about Satiety totally explained
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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.
Structure
CCK is composed of varying numbers of
amino acids (for example, 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 Function
CCK mediates a number of
physiological processes, including
digestion and
satiety.
Digestion
Secretion 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.
Neurobiology
As 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.
Further Information
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