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L-trp (zeige TBPL1 Proteine) is a luminal regulator of CCK release with effects on gastric emptying, an effect that could be mediated by CCK. L-trp's effect on GLP-1 (zeige GCG Proteine) secretion is only minor. At the doses given, the two amino acids did not affect subjective appetite feelings.
The CCK polymorphism have reported significant association of -45C>T polymorphism with the presence of hallucinations.
CCK does not appear to play a unique independent role in satiety/satiation.
CCK release has been found to be halved in pregnant women with hyperemesis gravidarium, which supports the hypothesis that gastrointestinal motility is increased in pregnant women with hyperemesis gravidarium.
CCK in plasma is an independent marker of cardiovascular mortality in elderly female patients.
These data offer preliminary evidence supporting an association between the rs1799923 polymorphism in the CCK gene and PTSD
Data suggest that endocrine responses differ between jejunal and gastric enteral feeding, with higher peak plasma CCK (cholecystokinin), PYY (peptide YY), and GLP-1/2 (glucagon-like peptides 1/2) concentrations being attained after jejunal feeding.
active GLP-1 (zeige GCG Proteine) produced in the islet stimulates cholecystokinin production and secretion in a paracrine manner via cyclic AMP (zeige APRT Proteine) and CREB (zeige CREB1 Proteine).
Cardiac expression of pro-cholecystokinin is cell-specific, which differentiates the expression from that of intestinal endocrine cells and cerebral neurons. Plasma Pro-CCK is a prognostic marker in patients with stable heart failure.
CCK binding modulates the contractile function of the lower esophageal sphincter through differential binding to the CCK-A receptor on the sling and clasp (zeige CLASRP Proteine) fibers
RIP2-knockout attenuates cardiac injury and dysfunction in hypertrophic heart. RIP2-deficience alleviates inflammation in heart of hypertrophic mice. RIP2-deletion inhibits fibrosis in the heart of hypertrophic mice.
CCK/GLP-1 (zeige GCG Proteine) play contributory roles in anorexia induction by trichothecenes T-2 toxin, HT-2 toxin, diacetoxyscirpenol and neosolaniol.
GPR120-induced incretin glucse-dependent insulinotropic polypeptide secretion is indirectly mediated by cholecystokinin.
Medullary interstitial cells respond to body fluid expansion by CCK release for feedback regulation of the late proximal tubular reabsorption.
results suggest that normal integration of CCK+ basket cells in cortical networks is key to support spatial coding in the hippocampus.
this study reveals that LRRK2 is a new positive regulator of Rip2 and promotes inflammatory cytokine induction through the Nod1/2-Rip2 pathway.
PC7 (zeige PCSK7 Proteine) has a critical role in normal processing of cholecystokinin in mouse brain
These studies reemphasize the beneficial effects imparted by co-administration of obestatin and CCK8 and their potential use towards countering obesity.
that Rip2 modifies VEGF-induced signalling and vascular permeability in myocardial ischaemia
new information on the cell specific localization of NUCB2/nesfatin-1 (zeige NUCB2 Proteine) in the intestinal mucosa, and a novel function for nesfatin-1 (zeige NUCB2 Proteine) in modulating intestinal CCK and PYY expression and secretion
We conclude that only a small fraction of neuronal CCK is nonsulfated. The intracellular distribution of nonsulfated CCK in neurons suggests that they contribute only modestly to the CCK transmitter activity.
Cardiac expression of pro-cholecystokinin is cell-specific, which differentiates the expression from that of intestinal endocrine cells and cerebral neurons.
This review explores the role of luminal cholecystokinin on the regulation of exocrine pancreatic secretion in author's studies of neonatal pigs.
This review explores the role of luminal cholecystokinin on the regulation of exocrine pancreatic secretion in author's studies of newborn calves.
Cholecystokinin is a brain/gut peptide. In the gut, it induces the release of pancreatic enzymes and the contraction of the gallbladder. In the brain, its physiologic role is unclear. The cholecystokinin pro-hormone is processed by endo- and exo-proteolytic cleavages. Two transcript variants encoding the same protein have been found for this gene.
, cholecystokinin triacontatriapeptide
, receptor-interacting serine/threonine-protein kinase 2
, tyrosine-protein kinase RIPK2