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- “In 1973, Gibbs et al. discovered that exogenous CCK inhibits food intake (92).
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The concentration increases within 20 min to 3–5 pmol/l during meal stimulation, and then declines gradually only to reach a second peak after 1.5–2 hours. In comparison with most other pancreatic and gastrointestinal hormones (62), the concentrations of CCK in plasma are low. When food-induced CCK in plasma is mimicked by infusion of exogenous CCK, the same degree of gallbladder contraction and release of enzymes as seen during meals occurs (54, 62–64). Therefore, the low circulating concentrations of CCK are sufficient to account for the gallbladder contraction and pancreatic enzyme secretion during meals. The major sites of CCK expression are as mentioned endocrine cells in the gut, the brain, and in peripheral nerves.
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Gut hormones have various physiological functions that include specifically targeting the brain to regulate appetite. New research suggests that gut hormones can be used to specifically regulate energy homeostasis in humans, and offer a target for anti-obesity drugs. In rodent kidneys (rat, mice, and guinea pigs), CCK has recently been shown by immunohistochemistry to be expressed both in the renal cortex and in the medulla.
Adrenal medullary cells produce small amounts of CCK, although amidated and with a low degree of sulfation (98). The picture has varied (12) due to species differences and because the molecular pattern along the gut varies (59, 60). In man, CCK-33 predominates in plasma, but CCK-58, -22, and -8 are also present (11, 61). Moreover, cerebral CCK neurons are more abundant than neurons of other neuropeptides (42, 45, 46). While most peptidergic neurons occur in subcortical regions, CCK is expressed in the highest concentrations in neocortical neurons (39, 42, 47). The perikarya of the cortical CCK nerves are distributed in layers II–VI, with the highest frequency in layers II and III (42, 48).