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CCK — INS

Text-mined interactions from Literome

Abdel-Wahab et al., Biochim Biophys Acta 1999 : In acute ( 20 min ) incubations, 10 ( -10 ) mol/l CCK-8 enhanced insulin release by 1.2-1.5-fold at 5.6-11.1 mmol/l glucose ... At 5.6 mmol/l glucose, CCK-8 at concentrations ranging from 10 ( -11 ) to 10 ( -7 ) mol/l induced a significant 1.6-1.9-fold increase in insulin secretion
Simonsson et al., Biochem Biophys Res Commun 2000 : In parallel with effects on [ ( 3 ) H ] AA, the expected additive insulin secretion induced by mellitin or CCK-8 in combination with forskolin or GLP-1, respectively, was reduced
Zdrojewicz et al., Postepy Hig Med Dosw 2001 : Recent research shows that CCK increases insulin and glukagon secretion and activates hypothalamo-pituitary-adrenal axis
Ferrer et al., Dig Dis Sci 2001 : Effect of exogenous cholecystokinin and secretin on pancreatic secretion of insulin and glucagon in rats : in vivo model without hepatic filter
Davies et al., Int J Exp Diabetes Res 2001 (Body Weight...) : Insulin responses to glucagon-like peptide-1 ( 10 ( -9 ) mol/l ), cholecystokinin-8 ( 10 ( -8 ) mol/l ) and L-alanine ( 10 mmol/l ) were increased by 32 %, 31 % and 68 % respectively ( p < 0.05-0.01 ) ... However, the insulin secretory responses to glucose, glucagon-like peptide-1, cholecystokinin-8 and L-alanine were decreased after 40 days of re-culture to 65 %, 72 %, 73 % and 42 % respectively of the values before implantation ( p < 0.05-0.01 )
Rosenberg et al., Ann Surg 1976 (Hypoglycemia) : Atropine 0.2 mg/kg abolished the insulin response and at 0.4 mg/kg inhibited ( 50 % ) the enzyme response to cholecystokinin ; these effects were unaltered by antrectomy or antroneurolysis
Hosotani et al., J Cell Physiol 1992 : Insulin ( 167 nM ) did not affect the CCK stimulated amylase release or immunoreactive CCK in the media
Baum et al., Digestion 1992 : Role of endogenously released cholecystokinin in determining postprandial insulin levels in man : effects of loxiglumide, a specific cholecystokinin receptor antagonist
Verspohl et al., Peptides 1992 : The role of cholecystokinin ( CCK8 ) on glucose production and elimination, and on plasma insulin and glucose in rats
Karlsson et al., Eur J Pharmacol 1992 : The effects of the cholecystokinin A (CCKA) receptor antagonist, L-364,718, and the CCKB receptor antagonist, L-365,260, on CCK-8 stimulated insulin secretion were studied in vivo in the mouse ... It was found that CCK-8 stimulated insulin secretion was suppressed by L-364,718 at a low dose level ( 0.078 mumol/kg ) ... In contrast, L-365,260 caused a partial inhibition of CCK-8 stimulated insulin release only at the high dose level ( 24 mumol/kg ) ... It is concluded that the CCK-8 stimulated insulin release in vivo is mediated by CCK receptors of the CCKA subtype
Niederau et al., Pancreas 1992 : This study used a cholecystokinin (CCK) antagonist to evaluate whether CCK that is released after regular meals regulates meal stimulated insulin secretion ... Although the present study does not rule out that in some conditions CCK may increase insulin secretion in humans, the results do rule out that CCK acts as a major physiologic incretin in healthy humans
Kogire et al., Pancreas 1992 : Chronic effect of oral cholestyramine, a bile salt sequestrant, and exogenous cholecystokinin on insulin release in rats ... The absence of a stimulatory effect of cholestyramine and CCK administration on insulin release in response to CCK-8 may be related to a down-regulation of CCK receptors on beta cells
Kageyama et al., Regul Pept 2005 : These results show clearly that CCK-AR exists not only in B but also in A cells of the rat pancreas, suggesting that CCK regulates the secretion of insulin and glucagon at least partly via CCK-AR
Korc et al., Endocrinology 1991 : In acini, the CCK8 mediated increases in Ins ( 1,4,5 ) P3 and Ins ( 1,3,4,5 ) P4 levels were progressively greater as the extracellular calcium concentration was raised from the micromolar range to 1.28 mM and progressively smaller as the manganese concentration was raised from 10 microM to 1 mM
Ahrén et al., Diabetes Res Clin Pract 1991 : CCK-8 and GIP together ( 100 pmol/kg for both ) increased plasma levels of insulin , PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake ... We conclude that in man, both CCK-8 , CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon
Fehmann et al., Pancreas 1990 : In concentrations as they occur physiologically after a meal, CCK-8 alone had no significant effect on basal or glucose stimulated ( 6.7 mM ) insulin secretion
Fehmann et al., Biochim Biophys Acta 1991 : The priming effect of glucagon-like peptide-1 ( 7-36 ) amide ( GLP-1 ( 7-36 ) amide ), glucose dependent insulin releasing polypeptide ( GIP ) and cholecystokinin-8 (CCK-8) on glucose induced insulin secretion from rat pancreas was investigated
Milke García et al., Rev Gastroenterol Mex 2005 : Satiation biomarkers ( stop feeding ) are gastric distention and hormones ( CCK , GLP-1 ) and satiety biomarkers ( induce feeding ) are food induced thermogenesis, body temperature, glycaemia and also hormones ( insulin , leptin and ghrelin )
Paik et al., J Korean Med Sci 2007 (Body Weight...) : Peptide YY, cholecystokinin , insulin and ghrelin response to meal did not change, but mean serum levels of insulin is reduced in children with Prader-Willi syndrome
Pröfrock et al., Biochem Biophys Res Commun 1991 : In rat pancreatic acinar cells epidermal growth factor (EGF) and insulin increase both basal and cholecystokinin ( CCK-OP ) stimulated amylase release in vitro ( 1 ) as a long term function of this tissue
Karlsson et al., Acta Physiol Scand 1991 : Cholecystokinin stimulated insulin secretion and protein kinase C in rat pancreatic islets ... In isolated rat pancreatic islets, the possible involvement of protein kinase C in cholecystokinin-8 stimulated insulin secretion was investigated ... In normal islets, the protein kinase C-inhibitor, staurosporine, inhibited 12-O-tetradecanoyl phorbol 13-acetate- and glucose stimulated insulin secretion ( P less than 0.01 ), but was without effect on cholecystokinin-8 stimulated insulin release ... Furthermore, in normal islets, cholecystokinin-8 had no effect on insulin release at a low glucose level ( 3.3 mmol l-1 ) ... Furthermore, the lack of effect of cholecystokinin-8 on insulin secretion at a low glucose level might be explained by an insufficient activation of protein kinase C under these conditions
Kusagawa et al., Nihon Geka Gakkai Zasshi 1991 : On the other hand, in dogs without DM, pancreatic regeneration rate showed 42.7 % at 12 weeks, insulin release and pancreatic exocrine function had been recovered well, and plasma CCK levels increased without changes of gastric secretion
Fried et al., Diabetologia 1991 : Physiological role of cholecystokinin on postprandial insulin secretion and gastric meal emptying in man ... The aim of this investigation was therefore to clarify the role of endogenous cholecystokinin in the regulation of insulin release and gastric emptying applying the highly potent and specific cholecystokinin receptor antagonist loxiglumide
Hildebrand et al., J Clin Endocrinol Metab 1991 : We conclude that CCK receptor blockade with iv loxiglumide does not affect postprandial insulin secretion
Schmid et al., Clin Physiol Biochem 1990 : Composition of amino acid infusions and effect of cholecystokinin on insulin release in dogs ... In the present study we have examined if the different composition of intravenously administered amino acid solutions is of importance for the effect of cholecystokinin (CCK) on pancreatic insulin and glucagon release in dogs
Okabayashi et al., Am J Physiol 1990 : Regulatory effect of cholecystokinin on subsequent insulin binding to pancreatic acini ... We investigated the regulatory effect of cholecystokinin (CCK) on subsequent insulin binding to pancreatic acinar cells ... In pancreatic membrane prepared from acini preincubated with 100 pM CCK-8 for 120 min at 37 degrees C, displacement of 125I-insulin ( 83 pM ) by unlabeled insulin ( 24 degrees C, 1 h ) revealed that CCK-8 inhibited 125I-insulin binding by altering the receptor affinity of the high-affinity binding site ... In acinar preparations the inhibitory effect of CCK-8 on 125I-insulin binding was abolished when acini were preincubated with CCK-8 and CCK receptor antagonist L 374718 at 37 degrees C. ( ABSTRACT TRUNCATED AT 250 WORDS )
Schuppin et al., Regul Pept 1990 : In combination, CCK and CCh increased glucose stimulated insulin secretion by an amount equivalent to the sum of their individual increases
Lo et al., Diabetes 2011 (Glucose Intolerance...) : CCK is involved in regulating insulin secretion and glucose tolerance in mice eating an HFD
Okabayashi et al., Pancreas 1990 : Proglumide analogues CR 1409 and CR 1392 inhibit cholecystokinin stimulated insulin release more potently than exocrine secretion from the isolated perfused rat pancreas
Rosewicz et al., Digestion 1990 : In contrast, neither SBTI intraduodenally, nor intravenous CCK had any effects on mRNA levels of insulin , glucagon, PP or somatostatin
Shikado et al., Jpn J Physiol 1990 (Hyperglycemia) : Necessity of hyperglycemia for effects of endogenous cholecystokinin on insulin and pancreatic exocrine secretion in conscious rats ... The effects of endogenous cholecystokinin (CCK) on insulin and pancreatic exocrine secretion were examined in conscious rats
Woods et al., Am J Physiol Endocrinol Metab 2012 : For example, cholecystokinin (CCK) , a duodenal peptide secreted during meals that aids in digestion, also reduces ongoing food intake, thereby contributing to satiation ; and insulin and leptin, hormones secreted in direct proportion to body fat, act in the brain to help control adiposity by reducing energy intake
Meyer-Gerspach et al., J Clin Endocrinol Metab 2013 : Results : Within the first 60 minutes, high-concentration CDCA induced a small but significant increase in GLP-1 and CCK secretion ( P = .016 and P =.011 ), whereas plasma C-peptide, insulin , and glucose were not affected
Williams et al., Diabetes 1985 (Diabetes Mellitus...) : 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
Otsuki et al., Dig Dis Sci 1987 : The stimulatory effect of both cholecystokinin octapeptide and secretin on insulin secretion was also inhibited by pirenzepine
Lindskog et al., Horm Res 1988 : CCK-8 ( 6.3 nmol/kg ) or terbutaline ( 3.6 mumol/kg ) markedly increased the plasma insulin levels ... Galanin ( 4.0 nmol/kg ) completely abolished the insulin response to CCK-8 ( p less than 0.001 ), but pancreastatin ( 4.0 nmol/kg ) was without effect
Garry et al., Am J Physiol 1989 : Exogenous insulin ( 10 mU/ml ) significantly potentiated cholecystokinin- ( CCK ; 0.5 mU/ml ) stimulated amylase secretion ( 12.47 +/- 2.9 micrograms/ml, n = 7 )
Yamaguchi et al., Endocrinology 1989 : Glucose, alpha-ketoisocaproate ( KIC ), and sulfated cholecystokinin ( CCK8S ) increased insulin secretion and formation of [ 3H ] inositol phosphate, [ 3H ] inositol bisphosphate, and [ 3H ] inositol trisphosphate
Bodziony et al., Exp Clin Endocrinol 1989 (Atrophy) : However, the function of isolate islets did not change, as investigated by the basal or glucose stimulated secretion of insulin, glucagon and somatostatin, and by the CCK stimulated secretion of insulin
Karlsson et al., Acta Physiol Scand 1989 : At a low dose level, proglumide ( 28 mumol kg-1 ) inhibited selectively CCK-8 induced insulin and glucagon secretion ... CR 1409 inhibited CCK-8 induced insulin secretion at a high ( 21 mumol kg-1 ) but not at a low ( 0.21 mumol kg-1 ) dose level ... L-364,718 ( 2.4 mumol kg-1 ) inhibited both CCK-8 induced insulin and glucagon secretion
Peiró et al., Metabolism 1989 : Pancreastatin infusion consistently reduced the insulin responses to VIP, GIP, and 8-CCK without modifying glucagon or somatostatin release
Zawalich et al., Diabetologia 1989 : Combined tolbutamide and cholecystokinin led to a biphasic insulin secretory response which was significantly enhanced by addition of 50 mumol/l monooleoylglycerol, an inhibitor of diacylglycerol kinase
Schmid et al., Pancreas 1989 : Effect of CCK on insulin , glucagon, and pancreatic polypeptide levels in humans
Inui et al., Endocrinol Jpn 1989 : However, i.v. pancreastatin did inhibit the i.v. CCK-8 induced insulin but not PP release
Skoglund et al., Eur J Pharmacol 1987 : The elevated plasma insulin levels after injection of carbachol or terbutaline were lowered by clonidine but not by phenylephrine whereas the CCK-8 induced increase in plasma insulin levels was not affected by either clonidine or phenylephrine
Fujimura et al., Pancreas 1988 : At the lowest concentration of CGRP ( 10 ( -11 ) M ), the inhibitory effect of CGRP on CCK-8 stimulated release of insulin was statistically significant ( p less than 0.05 ) and exceptionally potent ( 65-90 % inhibition )
Kaminski et al., Am J Physiol 1988 : Of possible importance in the choleresis produced by CCK is the stimulation by exogenous CCK of glucagon and insulin release from the pancreas
Verspohl et al., Diabetes 1986 : When the effect of CCK on insulin release from the islets was studied, the order of potency of CCK agonists and antagonists on insulin secretion was the same as the order of their ability to inhibit 125I-CCK binding ... The effect of CCK on insulin secretion was dependent on the glucose concentration in the media
Della-Fera et al., Prog Clin Biol Res 1985 : Little is known of CCK 's mechanisms of action, but because CNS CCK also causes changes in both gut motility and secretion of insulin and glucagon, the satiety could result directly from effects on behavior, and indirectly through metabolic changes
Otsuki et al., Endocrinology 1986 : Since CCK is released by meal intake and exogenous CCK stimulates insulin release and augments glucose induced insulin release, it is possible that endogenous CCK plays an important role in the enteroinsular axis ... The present findings of blockade of CCK-8 induced insulin release by selective antagonist of the action of CCK provide evidence for CCK as a mediator in the enteroinsular axis
Zawalich et al., Diabetes 1987 : The effects of sulfated cholecystokinin ( CCK-8S ) and glucose on insulin secretion and polyphosphoinositide ( PPI ) metabolism were studied in isolated rat islets ... Furthermore, the effects of CCK-8S on PPI and Ca2+ metabolism are observed whether islets are incubated in either 2.75 or 7 mM glucose, but CCK-8S only stimulates insulin secretion ( a biphasic response ) when the higher glucose concentration is present
Verspohl et al., Regul Pept 1987 : In rat pancreatic islets the effects of cholecystokinin-8 (CCK8) on glucose mediated insulin release, 45Ca2+ net uptake, 45Ca2+ efflux, 86Rb+ efflux, cAMP- and cGMP levels were studied ... In the presence of a substimulatory glucose concentration ( 3 mM ) CCK8 concentrations of up to 1 microM had no effect on insulin release, but CCK8 at 10 nM potentiated the stimulatory effect of glucose ( 11.1 mM )
Sandberg et al., Pharmacol Toxicol 1988 : We found that CCK-33, CCK-8 and CCK-7 ( 1 nM ) all significantly stimulated insulin secretion in the presence of 4.4 mM or 6.7 mM glucose ... In contrast, CCK-4 , CCK-6 and CCK-33 ( 1-21 ) had no effect on insulin secretion
Zawalich et al., Diabetes 1988 : L 364718, at levels 10- to 100-fold greater than those necessary to attenuate CCK-8S induced insulin secretion, had no adverse effect on the insulin secretory response of freshly isolated islets to 10 mM glucose alone, 5 mM D-glyceraldehyde, 15 mM alpha-ketoisocaproate, or 50 ng/ml gastric inhibitory polypeptide
Otsuki et al., Pancreas 1988 : Effects of hydrocortisone on glucose- and cholecystokinin induced insulin release from the isolated perfused rat pancreas ... The insulin response to 100 pM cholecystokinin ( CCK-8 ) was also significantly higher in the hydrocortisone treated rats than in the control group ... Hydrocortisone ( 17-hydroxycorticosterone ) at a concentration of 100 microM caused significant inhibition of the stimulatory effect of CCK-8 on insulin secretion ... We have demonstrated in this study a dual effect of hydrocortisone on insulin release : first, the potentiation of the insulin secretion stimulated by glucose but not by CCK-8 and, second, the inhibition of CCK-8 stimulated insulin secretion
Inui et al., Peptides 1988 : Intravenous CCK-8 also stimulated PP and insulin release, through mechanisms that were atropine-sensitive and atropine-insensitive, respectively
Verspohl et al., Eur J Pharmacol 1988 : Proglumide antagonizes cholecystokinin effects on plasma glucose and insulin in rats in vivo
Ishizuka et al., Pancreas 1988 : CCK-8 ( greater than 10 ( -8 ) M ) also increased glucose stimulated release of insulin from newborn islet cells, however its effect was not significant and not as strong as that observed with adult islet cells
Sandberg et al., Acta Endocrinol (Copenh) 1988 : Gastric inhibitory polypeptide (GIP), cholecystokinin (CCK) , and vasoactive intestinal polypeptide (VIP) stimulate insulin secretion ... In summary 1 ) GIP, CCK-33 and VIP all potentiate glucose induced insulin secretion from the perfused rat pancreas, and 2 ) CCK-33 potentiates and VIP inhibits GIP induced insulin secretion
Rushakoff et al., J Clin Endocrinol Metab 1987 : In addition, infusion of a mixture of amino acids with and without concomitant CCK infusions revealed that CCK potentiated the insulin release induced by mixed amino acids ... In contrast to the potent effect of CCK on amino acid induced insulin release, infusions of CCK together with glucose caused no enhancement of glucose stimulated insulin release
Rossetti et al., Diabetes 1987 : Physiological role of cholecystokinin in meal induced insulin secretion in conscious rats
Reagan et al., Eur J Pharmacol 1987 : Fasting and L-364,718 prevent cholecystokinin induced elevations of plasma insulin levels ... In conclusion, CCK produces a nutrition dependent increase in plasma insulin levels in vivo via an action upon peripheral CCK receptors
Ahrén et al., Acta Pharmacol Toxicol (Copenh) 1986 : When injecting CCK-8, CCK-33 or CCK-39 at dose levels substimulatory on basal insulin secretion ( 0.53 nmol/kg ), together with glucose, CCK-39 potentiated glucose induced insulin secretion whereas CCK-8 and CCK-33 were without effects ... In contrast, at the higher dose level of 5.3 nmol/kg, CCK-8 , CCK-33, and CCK-39 all potentiated glucose induced insulin secretion
Zawalich et al., Endocrinology 1986 : The results support a role for CCK8S in the regulation of insulin levels in vivo
Inui et al., Nihon Naibunpi Gakkai Zasshi 1985 : The integrated insulin responses to MSF, IV-Glucose and IV-CCK-8 were 28, 58 and 30 %, respectively, as those of controls ... Prior transthoracic bilateral truncal vagotomy abolished the suppressive effect of PP on glucose- and CCK-8 induced insulin secretion
Pederson et al., Can J Physiol Pharmacol 1979 : Although 50 % as potent as GIP on a weight basis and 43 % as potent on a molar basis, the insulin response to CCK was multiphasic and sustained for the duration of the infusion
Schusdziarra et al., Neuropeptides 1984 : CCK-8NS reduced glucose stimulated insulin release already at the lowest dose of 50 pmol/kg
Ahrén et al., Acta Endocrinol (Copenh) 1981 (Hyperthyroidism...) : Insulin response to CCK-8 and carbachol was less enhanced, by about 100 and 50 %, respectively
Ahrén et al., Acta Endocrinol (Copenh) 1983 : GIP and CCK-8 , when injected in threshold doses not affecting basal insulin secretion, did markedly enhance basal insulin release when given simultaneously ... Insulin release stimulated by a half-maximal dose of L-IPNA was not affected by either GIP or CCK-8 at the threshold doses
Hermansen et al., Endocrinology 1984 : CCK-4 and CCK-8 at concentrations of 1, 10, and 100 nM dose dependently stimulated pancreatic SRIF, insulin , and glucagon release
Hermansen et al., Endocrinology 1980 : Insulin release was enhanced by substance P ( 150 +/- 45 % ; P less than 0.05 ), bombesin ( 162 +/- 56 % ; P less than 0.05 ), VIP ( 44 +/- 5 % ; P less than 0.01 ), and CCK-8-S ( 190 +/- 17 % ; P less than 0.001 )
Sakamoto et al., Endocrinology 1982 : CCK ( 0.25 mU/ml ) or caerulein ( 0.01 ng/ml ) potentiated the insulin secretion induced by 5.6 mM glucose ; a significant increase in pancreatic exocrine secretion was also observed at these doses of CCK or caerulein ... Thus, CCK or caerulein significantly and coincidentally stimulated both insulin secretion and pancreatic exocrine function if 5.6 mM or more glucose is present, whereas in previous studies using 2.8 mM glucose, stimulation of insulin secretion was elicited only with concentrations of the peptides supramaximal for an effect on pancreatic exocrine secretion
Okabayashi et al., Endocrinology 1983 : The present observations suggest that the structural requirements for CCK induced insulin secretion are the same as those for CCK induced exocrine secretions, and that the amino acids in position 5-8 and the amidated residue on the C-terminus are required for physiological activity of CCK on both the exocrine and endocrine pancreas
Ahrén et al., Acta Diabetol Lat 1981 : The insulin-secretory response to CCK-39 and CCK-8 in the absence of other secretagogues was partially abolished by pretreatment with the cholinergic blocker methylatropine as well as with the beta-adrenoceptor blocker L-propranolol
Korc et al., Proc Natl Acad Sci U S A 1984 : CCK8 did not inhibit the binding of 125I labeled insulin to pancreatic acini
Potau et al., Biochem Biophys Res Commun 1984 : In contrast to its effects on IGF II binding to acini, CCK8 had only small effects on IGF I binding and no effects on insulin binding
Metzger et al., Physiol Behav 1983 : CCK-8 inhibited feeding and delayed the plasma glucose and insulin response to a mixed-meal ... There was no evidence that CCK-8 stimulated insulin release, nor was the usual close relationship between plasma glucose and insulin levels in response to a mixed-meal changed by CCK-8
Fujimoto et al., Horm Metab Res 1981 : Only glucagon ( 14 nM ), GIP ( 10 and 20 nM ), and CCK-OP ( 20 nM ) enhanced glucose stimulated insulin release during a 60-min incubation period
Jensen et al., Acta Physiol Scand 1981 : CCK-33 and -8 did not stimulate the secretion of insulin significantly, and neither of the cholecystokinins increased the secretion of glucagon and bicarbonate
Kihara et al., Pancreas 1995 : FK480 and KSG-504 inhibited CCK-8 stimulated pancreatic juice flow, protein output, and insulin release in a dose dependent manner ... Both antagonists inhibited CCK-8 stimulated insulin release more potently than exocrine secretion
Malm et al., Scand J Clin Lab Invest 1993 : This effect of CCK did not require extracellular Ca2+, was not inhibited by somatostatin ( 100 nmol l-1 ), and no concomitant increase in the insulin secretion was observed ... At 12 mmol l-1 glucose, the phospholipase C activity and the insulin secretion were potentiated by CCK ... Moreover, whereas the CCK induced increase in the phospholipase C activity was unaffected, verapamil blocked the CCK induced increase in the insulin secretion
Kimura et al., Jpn J Pharmacol 1994 : These results demonstrate that CCK-8 stimulated insulin release only at high glucose level is glucose dependent
Mineo et al., Res Vet Sci 1994 : The effects of cholecystokinin-8 (CCK-8) and pentagastrin on insulin and glucagon secretion were studied in conscious sheep
Giaever et al., Int J Cancer 1993 : In normal pancreatic islets, pertussis toxin inhibited the CCK induced increase in Ins-1,4,5-P3 , whereas no effect was seen at 3.3 mM glucose
Fridolf et al., Biochem Biophys Res Commun 1993 : Role of extracellular Na+ on CCK-8 induced insulin secretion ... CCK-8 stimulates insulin secretion by an effect involving phosphoinositide ( PI ) hydrolysis and release of Ca2+ from intracellular stores ... CCK-8 ( 100 nM ) stimulated insulin secretion from isolated rat islets ... Thus, the present study shows that both the second phase of CCK-8 stimulated insulin secretion and the CCK-8 stimulated postpeak reduction in [ Ca2+ ] IC are dependent on extracellular Na+
Okabayashi et al., Nihon Shokakibyo Gakkai Zasshi 1993 (Pancreatic Neoplasms) : [ Effect of cholecystokinin and secretin on insulin binding to rat pancreatic acini and pancreatic cancer cell line AR42J cells ] ... In order to clarify the interaction of hormones which exert various effects on the exocrine pancreas, we investigated the effect of cholecystokinin (CCK) and secretin on subsequent insulin binding to pancreatic acini and cultured AR42J cells derived from azaserine induced acinar cell carcinoma of the pancreas ... In addition, secretin exerted no potentiating effect on the inhibitory effect of CCK on 125I-insulin binding to pancreatic acini ... Based on these results, we further investigated the effect of CCK and TPA on subsequent 125I-insulin binding to AR42J cells ... In this carcinoma cell line, inhibitory effect of CCK and TPA on insulin binding was completely abolished
Salas et al., Diabete Metab 1995 : Amylin significantly inhibited insulin response to BAY K 8644 ( 65 % ), KCI ( 60 % ) and 8-CCK ( 80 % ) as well as the early phase of tolbutamide induced insulin output ( 70 % )
Hasegawa et al., Metabolism 1996 (Diabetes Mellitus, Type 2) : These results suggest a possible effect of CCK on insulin release in humans, and that the CCK secretory response to glucose in well controlled diabetic patients is not significantly altered
Lundquist et al., Endocrinology 1996 : In contrast, receptor activated insulin secretion induced by the insulinotropic hormone cholecystokinin ( CCK-8 ) was unaffected by the drug
Hirschberg et al., Contraception 1996 : Cholecystokinin stimulates the release of insulin and stimulates lipolysis in adipose tissue
Simonsson et al., Regul Pept 1996 : Involvement of phospholipase A2 and arachidonic acid in cholecystokinin-8 induced insulin secretion in rat islets ... However, the cyclooxygenase inhibitors, indomethacin ( 30 microM ) and salicylate ( 1.25 mM ) as well as the lipoxygenase inhibitors baicalein ( 1-100 microM ) and esculetin ( 0.5-50 microM ), did not affect CCK-8 induced insulin secretion ... We conclude that CCK-8 induced insulin secretion is partially mediated by a pathway involving PLA2, and that the formed AA, rather than its metabolites, is of importance
Lee et al., Pancreas 1996 : The role of insulin in the interaction of secretin and cholecystokinin in exocrine secretion of the isolated perfused rat pancreas
Morin et al., Am J Physiol 1997 (Diabetes Mellitus, Experimental) : By contrast, the ability of 1.0 mM carbachol or 300 nM cholecystokinin to stimulate insulin secretion and InsP generation was still observed
Mineo et al., Res Vet Sci 1997 : These results indicate that CCK-A type receptors rather than CCK-B receptors may be involved in CCK induced insulin secretion in sheep
Mineo et al., Comp Biochem Physiol A Physiol 1997 : The antagonistic effects of proglumide occurred in a dose dependent manner, and proglumide infusion at dose of 20 mumol/kg/min or above simultaneously inhibited CCK-8 induced amylase and insulin responses
Smeets et al., Br J Pharmacol 1998 : 5. In contrast, TPA evoked a rightward shift of the dose-response curve for CCK-8 induced Ins ( 1,4,5 ) P3 formation in both cell lines ... This demonstrates that high-level PKC activation inhibits CCK-8 induced Ins ( 1,4,5 ) P3 formation also at a post-receptor site
Simonsson et al., Diabetes 1998 : Insulin secretion induced by cholecystokinin-8 (CCK-8) was recently suggested to involve phospholipase A2 (PLA2) activation ... Neither the Ca2+ channel antagonist verapamil ( 100 micromol/l ) nor the Ca2+ATPase inhibitor thapsigargin ( 1 micromol/l ) affected CCK-8 induced AA efflux and insulin secretion ... Furthermore, despite removal of extracellular Ca2+, CCK-8 still increased AA efflux ( 48 +/- 14 % ; P = 0.006 ) and insulin secretion ( 105 +/- 46 % ; P = 0.025 ) ... We found that CCK-8 ( 100 nmol/l ; 5.6 mmol/l glucose ) induces lysophosphatidylcholine accumulation from [ 3H ] palmitate prelabeled islets ( 170 +/- 39 % ; P = 0.003 ) as well as arachidonic acid ( AA ) efflux from [ 3H ] AA-prelabeled islets ( 190 +/- 13 % ; P < 0.001 ), and that p-amylcinnamoylantranilic acid ( ACA ) ( 50 micromol/l ) -mediated PLA2 inhibition reduces CCK-8 induced AA efflux ( 52 +/- 11 % ; P = 0.001 ) and insulin secretion ( 67 +/- 16 % ; P < 0.001 ) ... Overnight protein kinase C ( PKC ) downregulation by 12-O-tetradecanoyl phorbol-13-acetate ( TPA ) ( 500 nmol/l ) reduced CCK-8 induced AA efflux ( 45 +/- 12 % ; P = 0.003 ) and insulin secretion ( 40 +/- 16 % ; P = 0.020 )
Karlsson et al., Regul Pept 1998 (Insulinoma) : In RINm5F cells, insulin release was not significantly affected by cholecystokinin (CCK)-8-S ( 10 ( -13 ) to 10 ( -7 ) M ), which is in contrast to the insulinotropic effect of CCK-8-S in normal rat islets ... There is, however, a functional difference between normal islets and the RINm5F cells with respect to effects of CCK-8-S on insulin release and [ Ca2+ ] ic