Ignet

Gene Information

Gene symbol: CCK

Gene name: cholecystokinin

HGNC ID: 1569

Related Genes

#	Gene Symbol	Number of hits
1	AGRP	1 hits
2	AKT1	1 hits
3	AR	1 hits
4	CASR	1 hits
5	CBL	1 hits
6	CCKAR	1 hits
7	CCKBR	1 hits
8	CCNA2	1 hits
9	CCND2	1 hits
10	CCND3	1 hits
11	CDK4	1 hits
12	CDK6	1 hits
13	FFAR1	1 hits
14	GAL	1 hits
15	GAST	1 hits
16	GHRL	1 hits
17	GIP	1 hits
18	GPR120	1 hits
19	GRP	1 hits
20	INS	1 hits
21	LEP	1 hits
22	NGF	1 hits
23	NPY	1 hits
24	NTS	1 hits
25	PRKCA	1 hits
26	PTK2	1 hits
27	PTK2B	1 hits
28	PYY	1 hits
29	RBL2	1 hits
30	SHC1	1 hits
31	SST	1 hits
32	TH	1 hits
33	VIP	1 hits

Related Sentences

#	PMID	Sentence
1	6124374	For instance, cholecystokinin and human pancreatic polypeptide (hPP) may be importantly involved in the regulation of appetite and satiety control and the development of obesity whereas somatostatin, "endorphins", and neurotensin may directly or indirectly modulate islet hormone secretion.
2	2412919	Isolated rat and mouse acini have insulin receptors, and in these cells, after binding to its receptors, insulin regulates a number of functions including: sugar transport, protein synthesis, and the number of cholecystokinin receptors.
3	3308589	It has been suggested that the gut hormone cholecystokinin (CCK), by modulating insulin output from pancreatic beta-cells, plays an important role in the enteroinsular axis.
4	2894431	The effect of proglumide ((+/-)-4-benzamido-N,N-dipropyl-glutaramic acid), a gastrin and cholecystokinin receptor antagonist, has been studied on the fasting plasma glucose (FPG) and insulin levels in normal and alloxan-diabetic mice.
5	2465695	When guinea pig pancreatic acini are first incubated with the COOH-terminal octapeptide of cholecystokinin (CCK-8), washed, and then reincubated with 125I-[Tyr4]bombesin (125I-[Tyr4]BN) there is a significant decrease in binding of 125I-[Tyr4]BN compared with that observed with pancreatic acini that have been first incubated with no additions.
6	2473654	In the present study we examined the effect of gastrin, the COOH-terminal octapeptide of CCK (CCK-8), and the tetrapeptide of CCK (CG-4) on contraction of dispersed gastric smooth muscle cells from guinea pig and tested the ability of various CCK receptor antagonists to affect agonist-induced muscle cell contraction.
7	2473654	Inhibition by each of the antagonists was competitive in nature, specific for CCK peptides, and each had the same IC50 whether contraction was stimulated by CCK-8, gastrin, or CG-4.
8	2502884	Experiments on rats using the primary monolayer culture of isolated islet cells proved that insulin secretion is directly modulated by the growth hormone (GH), C-terminal tetrapeptide of cholecystokinin, thyroliberin, and met-enkephalin, and by certain blood plasma factors of diabetes I patients.
9	2485904	The effect of cholecystokinin (CCK-33) and its fragments, C-terminal octapeptide (CCK-8) and C-terminal tetrapeptide (CCK-4), on arterial blood pressure and on the function of the isolated rat heart was studied in three groups of animals: normal (C group), rats with streptozotocin-induced diabetes of one month's duration (DM group) and with diabetes treated with insulin (DMI group).
10	1689117	First incubating guinea pig pancreatic acini with carbachol reduced the subsequent stimulation of amylase release caused by carbachol, cholecystokinin octapeptide (CCK-8), and bombesin but not that caused by vasoactive intestinal peptide, substance P, 8-bromoadenosine 3',5'-cyclic monophosphate, A23187, or 12-O-tetradecanoylphorbol-13-acetate.
11	1689117	Acini possess a single class of bombesin receptors, and first incubating acini with carbachol caused a 40% decrease in the number of bombesin receptors with no change in their affinity for bombesin. 12-O-tetradecanoyl phorbol-13-acetate reproduced the action of carbachol on binding of N-[3H]methylscopolamine and 125I-CCK-8 but not on binding of 125I-[Tyr4]bombesin, suggesting that carbachol activation of protein kinase C may in some way mediate the effect of carbachol on receptors for carbachol and those for CCK but not that on receptors for bombesin.
12	2189762	Only very high concentrations of CCK-8 (15 micrograms.kg-1.20 min-1) produced a small increase in plasma insulin levels, indicating a strong CCK-8-eliminating mechanism in the liver.
13	2192849	Cholecystokinin (CCK) and acetylcholine activate the hydrolysis of polyphosphoinositides, and gastric inhibitory polypeptide (GIP) and glucagonlike peptide 1 activate adenylate cyclase.
14	1702423	[psi 4,5]Secretin did not interact with cholecystokinin, bombesin, calcitonin gene-related peptide, or cholinergic receptors but did interact with receptors for vasoactive intestinal peptide, causing half-maximal inhibition at 72 microM and thus had a 18-fold higher affinity for secretin than vasoactive intestinal peptide receptors.
15	1745688	We conclude that hypnogenic and food-intake-reducing effects of exogenously administered CCK are closely associated; however, pancreatic insulin does not play a significant role in either of these effects.
16	1480583	Model experiments with primary monolayer cultures of isolated islet cells have helped demonstrate a direct insulinotropic effect of STH, TRH, C-terminal tetrapeptide cholecystokinin, opioid peptides and blood plasma of patients with insulin-dependent diabetes mellitus.
17	9176170	By contrast, the ability of 1.0 mM carbachol or 300 nM cholecystokinin to stimulate insulin secretion and InsP generation was still observed.
18	10657511	Neuropeptide Y (NPY), melanin concentrating hormone (MCH), orexins A and B, galanin, and agouti -related peptide (AgRP) all act to stimulate feeding while alpha-melanocyte stimulating hormone (alphaMSH), corticotropin releasing hormone (CRH), cholecystokinin (CCK), cocaine and amphetamine regulated transcript (CART), neurotensin, glucagon-like peptide 1 (GLP 1), and bombesin have anorectic actions.(1) Leptin, expressed in the periphery in white adipose tissue, acts in the CNS to modulate the expression of several of these hypothalamic peptides.(1) This creates a functional link between the adipose tissue and the brain that translates the information on body fat provided by leptin to input into energy balance regulating processes.
19	11961490	To investigate the effect of endogenous somatostatin on the interaction between endogenous insulin and exogenous cholecystokinin (CCK) in exocrine secretion of the totally isolated, perfused rat pancreas.
20	11961490	Glucose (18 mM) enhanced CCK (10 pM)-stimulated secretions of fluid and amylase in the normal pancreas, which was further elevated by a somatostatin antagonist.
21	11961490	Exogenous insulin (100 nM) also enhanced CCK-stimulated secretions in the streptozotocin-treated pancreas, which was also markedly increased by the somatostatin antagonist.
22	11961490	The glucose (18 mM)-enhanced CCK-stimulated secretions were much higher in the cysteamine-treated pancreas than in the normal pancreas, which was dose-dependently reduced by exogenous somatostatin (30, 100 pM).
23	12769602	It has been demonstrated that CCK-8 counteracts neuronal deficit following chemical or surgical lesions in both the central and peripheral nervous systems and that Nerve Growth factor (NGF) is involved in the CCK-induced recovery process.
24	12829630	Some of the actions of leptin depend on cholecystokinin (CCK).
25	12829630	However, it is unknown whether leptin modulates the release of CCK.
26	12829630	Here, we demonstrate in vitro that leptin induces the phosphorylation of extracellular signal-related kinase (ERK)-1/2 proteins and increases CCK release (EC(50) = 0.23 nmol/l) in CCK-secreting STC-1 cells.
27	12829630	In vivo in the rat, duodenal infusion of leptin increased plasma CCK at levels comparable to those induced by feeding.
28	12829630	Moreover, meal-induced increases in plasma CCK were markedly reduced in obese fa/fa rats, whereas the mobilization of the gastric leptin pool was similar in lean and obese Zucker rats.
29	14517799	Both cholecystokinin (CCK)-A and CCK-B receptors are expressed in the pancreas, and exogenous gastrin administration stimulates glucagon secretion from human islets.
30	16320257	Finally, we examined the coexpression of GHSR with tyrosine hydroxylase and cholecystokinin and demonstrate a high degree of GHSR mRNA expression within dopaminergic, cholecystokinin-containing neurons of the substantia nigra and ventral tegmental area.
31	16935329	The structure and function of many hypothalamic peptides (neuropeptide Y (NPY), melanocortins, agouti-related peptide (AGRP), cocaine and amphetamine regulated transcript (CART), melanin concentrating hormone (MCH), orexins have been characterized in rodent models The peripheral neuropeptides such as cholecystokinin (CCK), ghrelin, peptide YY (PYY3-36), amylin, bombesin regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake.
32	18845673	Glucose-stimulated insulin secretion was unaffected by CCK expression.
33	18845673	Analysis of cyclin and cdk mRNA and protein abundance revealed that CCK overexpression increased cyclin A, cyclin B, cyclin E, cdk1, and cdk2 with no change in cyclin D1, cyclin D2, cyclin D3, cdk4, or cdk6 in mouse and human islets.
34	20471368	The newly discovered G protein-coupled receptor GPR120 has recently been shown to stimulate secretion of the gut hormones glucagon-like peptide-1 and cholecystokinin upon binding of free fatty acids, thrusting it to the forefront of drug discovery efforts for treatment of type 2 diabetes as well as satiety and obesity.
35	21252045	The extracellular calcium-sensing receptor (CaSR) has recently been recognized as an L-amino acid sensor and has been implicated in mediating cholecystokinin (CCK) secretion in response to aromatic amino acids.
36	21252045	Fluorescence-activated cell sorting of duodenal I cells from CCK-enhanced green fluorescent protein (eGFP) transgenic mice demonstrated CaSR gene expression.
37	21252045	In fact, both secretagogues, as well as superphysiological Ca(2+), evoked an unexpected 20-30% decrease in CCK secretion compared with basal secretion in CaSR(-/-) CCK-eGFP cells.
38	10763483	The administration of CCK to intact animals causes increase of insulin content in endocrinocytes of pancreatic islets, but does not affect the level of hypoglycemia.
39	20955703	We sought to determine whether dietary fat-induced secretion of CCK is directly mediated by GPR40 expressed on I cells.
40	20955703	In contrast, in GPR40(-/-) that expressed eGFP, [Ca(2+)]i response to linoleic acid was reduced by 50% and there was no significant CCK secretion in response to linolenic acid.
41	20955703	In mice, olive oil gavage significantly increased plasma levels of CCK compared with pregavage levels: 5.7-fold in GPR40(+/+) mice and 3.1-fold in GPR40(-/-) mice.
42	20955703	Long-chain fatty acid receptor GPR40 induces secretion of CCK by I cells in response to dietary fat.
43	21602512	Cholecystokinin (CCK) is released in response to lipid intake and stimulates insulin secretion.
44	21602512	We hypothesized that CCK deficiency would alter the regulation of insulin secretion and glucose homeostasis.
45	21602512	CCK is involved in regulating insulin secretion and glucose tolerance in mice eating an HFD.
46	20534724	In summary, CCK is up-regulated by islet cells during obesity and functions as a paracrine or autocrine factor to increase beta-cell survival and expand beta-cell mass to compensate for obesity-induced insulin resistance.
47	21949903	Cholecystokinin, peptide YY, pancreatic polypeptide, glucagon-like peptide-1, and oxyntomodulin act through distinct yet synergistic mechanisms to suppress appetite, whereas ghrelin stimulates food intake.
48	16713446	CCK stimulated an association of Lyn with PKC-delta, Shc, p125(FAK) and PYK2 as well as with their autophosphorylated forms, but not with Cbl, p85, p130(CAS) or ERK 1/2.
49	21810446	Also CCK- and TPA-induced PKC? activation produced an increment in PKC?'s direct association with AKT, RafA, RafC and Lyn.
50	21984583	OBJECTIVE Metabolism of long-chain fatty acids within the duodenum leads to the activation of duodenal mucosal protein kinase C (PKC)-? and the cholecystokinin (CCK)-A receptor to lower glucose production through a neuronal network.
51	21984583	Conversely, molecular and pharmacological inhibition of duodenal PKC-? did not negate the ability of the duodenal CCK-A receptor agonist CCK-8 to lower glucose production, indicating that activation of duodenal PKC-? lies upstream (and not downstream) of CCK signaling.
52	21984583	CONCLUSIONS In summary, activation of duodenal PKC-? leads to the stimulation of CCK release and activation of the CCK-A receptor signaling axis to lower glucose production in normal rats, but fails to bypass duodenal CCK-resistance in high fat-fed rats.