Nonsulfated cholecystokinins in the small intestine of pigs and rats

Agersnap, Mikkel; Rehfeld, Jens F.

doi:10.1016/j.peptides.2015.07.010

Cited by 23 publications

(27 citation statements)

References 31 publications

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“…The endoproteolysis of proCCK occurs mainly at monobasic sites. Y-77 is mostly O-sulfated ( 16 – 20 , 40 ), which is decisive for CCK 1 receptor binding .…”

Section: Biogenesismentioning

confidence: 99%

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Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

2017

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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 CCK1 and CCK2 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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“…The endoproteolysis of proCCK occurs mainly at monobasic sites. Y-77 is mostly O-sulfated ( 16 – 20 , 40 ), which is decisive for CCK 1 receptor binding .…”

Section: Biogenesismentioning

confidence: 99%

“…Of particular importance is the tyrosyl residue in position seven [as counted from the C-terminus (Figure 1)]. The tyrosyl residue is rarely completely sulfated (16–20). The CCK 2 receptor binds sulfated and unsulfated ligands equally well, whereas the CCK 1 receptor is exclusive and requires Y-sulfation of the ligand.…”

Section: Introductionmentioning

confidence: 99%

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

2017

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“…This was unexpected because we anticipated that DJBS would prevent nutrients from coming into contact with the duodenal mucosa, which is rich in CCK‐secreting I cells, and thus, decrease postprandial CCK response, an important determinant of gallbladder emptying, as observed by de Jonge et al who used a comparable experimental design . The reason for this discrepancy remains unclear, but may relate either to variations in the tightness of the proximal anchoring of the DJBS or to the fact that not only the proximal but also the remaining jejunum houses numerous I cells . Additionally, the unaffected gallbladder motility could explain why we saw only one patient with gallbladder stone formation, which is in contrast to the 50% cumulative risk of gallstones following RYGB …”

Section: Discussionmentioning

confidence: 91%

“…18 The reason for this discrepancy remains unclear, but may relate either to variations in the tightness of the proximal anchoring of the DJBS or to the fact that not only the proximal but also the remaining jejunum houses numerous I cells. 37 Additionally, the unaffected gallbladder motility could explain why we saw only one patient with gallbladder stone formation, which is in contrast to the 50% cumulative risk of gallstones following RYGB. 12,38 What might have been the cause of the initial decrements in appetite and food intake among our NGT subjects?…”

Section: Metabolic Parameters Medication and Blood Pressurementioning

confidence: 90%

The impact of EndoBarrier gastrointestinal liner in obese patients with normal glucose tolerance and in patients with type 2 diabetes

Rohde

Federspiel

Vilmann

et al. 2016

Diabetes Obesity Metabolism

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“…Structurally, CCKs are defined as gallbladderemptying peptides having the C-terminal sequence Tyr-X 1 -X 2 -Trp-Met-Asp-Phe-NH 2, where X 1 in most mammals is a methionyl residue and X 2 a glycyl residue. Most bioactive CCK peptides are O-sulfated, but unsulfated CCK peptides also occur in normal tissue [17] and in tumor tissue [18], and they are natural agonists for the CCK B receptors.…”

Section: Definition Of the Cholecystokinin Family Of Peptidesmentioning

confidence: 99%

Cholecystokinin Expression in Tumors: Biogenetic and Diagnostic Implications

Rehfeld

2016

Future Oncol.

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Cholecystokinin (CCK) is a classic gut hormone. CCK is also a complex system of peptides expressed in several molecular forms in enteroendocrine I cells, in cerebral and peripheral neurons, in cardiac myocytes and spermatozoa. CCK gene expression has now been found at protein or peptide level in different neuroendocrine tumors; cerebral gliomas and astrocytomas and specific pediatric tumors. Tumor hypersecretion of CCK was recently reported in a patient with a metastatic islet cell tumor and hypercholecystokininemia resulting in a novel tumor syndrome, the cholecystokininoma syndrome. This review presents an overview of the cell-specific biogenesis of CCK peptides, and a description of the CCK expression in tumors and of the cholecystokininoma syndrome. Finally, assays for the diagnosis of CCK-producing tumors are reviewed.

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Nonsulfated cholecystokinins in the small intestine of pigs and rats

Cited by 23 publications

References 31 publications

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

The impact of EndoBarrier gastrointestinal liner in obese patients with normal glucose tolerance and in patients with type 2 diabetes

Cholecystokinin Expression in Tumors: Biogenetic and Diagnostic Implications

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