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2017 ; 8
(ä): 47
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Cholecystokinin-From Local Gut Hormone to Ubiquitous Messenger
#MMPMID28450850
Rehfeld JF
Front Endocrinol (Lausanne)
2017[]; 8
(ä): 47
PMID28450850
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Cholecystokinin (CCK) was discovered in 1928 in jejunal extracts as a gallbladder
contraction factor. It was later shown to be member of a peptide family, which
are all ligands for the CCK(1) and CCK(2) receptors. CCK peptides are known to be
synthetized in small intestinal endocrine I-cells and cerebral neurons. But in
addition, CCK is expressed in several endocrine glands (pituitary cells, thyroid
C-cells, pancreatic islets, the adrenals, and the testes); in peripheral nerves;
in cortical and medullary kidney cells; in cardial myocytes; and in cells of the
immune system. CCK peptides stimulate pancreatic enzyme secretion and growth,
gallbladder contraction, and gut motility, satiety and inhibit acid secretion
from the stomach. Moreover, they are major neurotransmitters in the brain and the
periphery. CCK peptides also stimulate calcitonin, insulin, and glucagon
secretion, and they may act as natriuretic peptides in the kidneys. CCK peptides
are derived from proCCK with a C-terminal bioactive YMGWMDFamide sequence, in
which the Y-residue is partly O-sulfated. The plasma forms are CCK-58, -33, -22,
and -8, whereas the small CCK-8 and -5 are potent neurotransmitters. Over the
last decades, CCK expression has also been encountered in tumors (neuroendocrine
tumors, cerebral astrocytomas, gliomas, acoustic neuromas, and specific pediatric
tumors). Recently, a metastastic islet cell tumor was found to cause a specific
CCKoma syndrome, suggesting that circulating CCK may be a useful tumor marker.
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