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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 (show GCG Proteins) produced in the islet stimulates cholecystokinin production and secretion in a paracrine manner via cyclic AMP (show APRT Proteins) and CREB (show CREB1 Proteins).
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 (show CLASRP Proteins) fibers
Data suggest that up-regulation of plasma CCK levels is 50% higher following breakfast of meal replacement beverage containing fat emulsion of rapeseed oil with droplet size of 0.1 um (versus 0.3 um); satiety response and food intake are unaffected.
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 (show NUCB2 Proteins) in the intestinal mucosa, and a novel function for nesfatin-1 (show NUCB2 Proteins) in modulating intestinal CCK and PYY expression and secretion
Results showed that CCK is important for lipid transport and energy expenditure to control body weight in response to dietary lipid feeding
SP1 (show SP1 Proteins) results in a CCK response deficiency that may contribute to the increased meal size and overall hyperphagia in synphillin-1 transgenic mice
serves as a novel positive modulator of ventricular remodelling after myocardial infarction via the regulation of NF-kappaB (show NFKB1 Proteins) and p38 (show CRK Proteins) signalling
active GLP-1 (show GCG Proteins) produced in the islet stimulates cholecystokinin production and secretion in a paracrine manner via cyclic AMP (show TMPRSS5 Proteins) and CREB (show CREB1 Proteins).
Data (including data from studies using transgenic mice) suggest that enhanced Cck expression in pancreatic beta-cells protects these cells from the cell-withering effects of aging, apoptotic stress, and (streptozotocin-induced) diabetes type 2.
Deoxynivalenol induced cholecystokinin and glucagon-like peptide 1 (show GCG Proteins) release by enteroendocrine cells in mediated by casR (show CASR Proteins)/TRPA1 (show TRPA1 Proteins) signaling.
Bacterial polysaccharide-responsive miR-150 and miR-143 RIPK2 and TAK1 to suppress NOD2-induced immunomodulators.
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