Interaction of Glucagon-like Peptide- 1 (7-36)amide and Cholecystokinin-8 in the Endocrine and Exocrine Rat Pancreas

Fehmann, Hans-Christoph; Göke, Burkhard; Weber, V.; Göke, Rüdiger; Trautmann, Michael E.; Richter, G.; Arnold, R.

doi:10.1097/00006676-199005000-00019

Cited by 34 publications

(23 citation statements)

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“…The mech anism of the synergistic interaction between GIP and ACh was beyond the scope of this study, although it has been suggested that a potentiating interaction between two secretagogues such as GIP and ACh, which act via different intracellular pathways, involves in teractions between the intracellular messen ger systems activated by those secretagogues [17]. With regard to this study, GIP stimu lated the production of cAMP in the p-cell [24], which has been proposed to sensitize the P-cell secretory mechanism to the AChstimulated increase in intracellular calcium [17], In agreement with this hypothesis, sim ilar synergistic interactions were recently re ported between GIP and CCK in perifused islets [39] and glucagon-like peptide-1 and CCK in the perfused pancreas [40],…”

Section: Discussionsupporting

confidence: 76%

Modulation of Acetylcholine-Stimulated Insulin Release by Glucose and Gastric Inhibitory Polypeptide

Verchere¹,

Kwok²,

Brown³

1991

Pharmacology

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The interactions of glucose, acetylcholine and gastric inhibitory polypeptide in the regulation of insulin secretion were examined using the in situ perfused rat pancreas. Acetylcholine (1 × 10^–6M) had no effect on the release of immunoreactive insulin in the presence of 2.2 × 10^–3M glucose. However, in the presence of 4.4, 6.6 or 8.9 × 10^–3M glucose, the same concentration of acetylcholine stimulated insulin secretion approximately fourfold. At the highest glucose concentration tested (17.8 × 10^–3M), the stimulatory effect of acetylcholine on insulin release was less pronounced. The insulin response to acetylcholine was potentiated by the presence of gastric inhibitory polypeptide. This potentiation was most marked when the peptide was present at a concentration of 1 × 10^–9M, whereas the effect of concomitant infusion of acetylcholine and 2 × 10^–10M gastric inhibitory polypeptide was only slightly greater than additive. Both atropine (1 × 10^–6M) and hexamethonium (1 × 10^–4M) inhibited the insulin response to acetylcholine. However, neither of these cholinergic antagonists had a significant effect on glucose- or gastric inhibitory polypeptide-stimulated insulin secretion. These results demonstrate that the insulinotropic action of acetylcholine is glucose-dependent. A synergistic interaction may exist between acetylcholine and gastric inhibitory polypeptide at the β-cell which does not involve glucose or gastric inhibitory polypeptide acting on cholinergic receptors in the pancreas. Cholinergic stimulation of insulin secretion in the perfused rat pancreas appears to be mediated by both muscarinic receptors on the β-cell and nicotinic receptors, presumably on intrapancreatic ganglia.

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Section: Discussionsupporting

confidence: 76%

Modulation of Acetylcholine-Stimulated Insulin Release by Glucose and Gastric Inhibitory Polypeptide

Verchere¹,

Kwok²,

Brown³

1991

Pharmacology

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“…From these findings, it was of interest to study the interaction of GLP-l(7-36) amide, CCK-8 and GIP on insulin secretion. The GLP-l(7-36) amide (5 x 1O-Io M) stimulated, glucose-induced (6.7 mM) insulin release from the perfused rat pancreas was potentiated by CCK-8 (maximal effect at 5 x lo-" M) [56] (Fig. 4).…”

Section: ( 4 ) Interaction Of Glp-1(7-36) Amide With Other Hormonesmentioning

confidence: 87%

“…4). Since the effect of GLP-l(7-36) amide is mediated by the adenylate cyclase system [23] the potentiation of the GLP-1 effect by CCK was explained by an interaction of different second messenger systems [56] as was suggested in the case of GIP and CCK [54]. Since both GLP-l(7-36) amide and GIP act via the adenylate cyclase system a combination of both revealed an additive synergistic effect which was only obtained when submaximal effective hormone concentrations were utilized [57].…”

Section: ( 4 ) Interaction Of Glp-1(7-36) Amide With Other Hormonesmentioning

confidence: 99%

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Glucagon‐like peptide‐1(7–36) amide is a new incretin/enterogastrone candidate

Göke

Fehmann

Göke

1991

Eur J Clin Investigation

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“…Fehmann and colleagues were the first to study the effect of GLP-1 on pancreatic acinar secretions (Fehmann et al, 1990). They examined the synergistic action of GLP-1 (10 pM) and cholecystokinin-8 (CCK-8, 1 nM-1 pM) on isolated rat pancreatic acini and found that GLP-1 had no impact on CCK-induced amylase secretion.…”

Section: Exocrine Pancreatic Secretionmentioning

confidence: 99%

Mechanisms of action of glucagon-like peptide 1 in the pancreas

Doyle

Egan

2007

Pharmacology & Therapeutics

583

465

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Glucagon-like peptide-1 is a hormone that is encoded in the proglucagon gene. It is mainly produced in enteroendocrine L cells of the gut and is secreted into the blood stream when food containing fat, protein hydrolysate and/or glucose enters the duodenum. Its particular effects on insulin and glucagon secretion have generated a flurry of research activity over the past twenty years culminating in a naturally occurring GLP-1 receptor agonist, exendin-4, now being used to treat type 2 diabetes. GLP-1 engages a specific G-protein coupled receptor that is present in tissues other than the pancreas (brain, kidney, lung, heart, major blood vessels). The most widely studied cell activated by GLP-1 is the insulin-secreting beta cell where its defining action is augmentation of glucose-induced insulin secretion. Upon GLP-1 receptor activation, adenylyl cyclase is activated and cAMP generated, leading, in turn, to cAMP-dependent activation of second messenger pathways, such as the PKA and Epac pathways. As well as short-term effects of enhancing glucose-induced insulin secretion, continuous GLP-1 receptor activation also increases insulin synthesis, and beta cell proliferation and neogenesis. Although these latter effects cannot be currently monitored in humans, there are substantial improvements in glucose tolerance and increases in both first phase and plateau phase insulin secretory responses in type 2 diabetic patients treated with exendin-4. This review we will focus on the effects resulting from GLP-1 receptor activation in islets of Langerhans

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Interaction of Glucagon-like Peptide- 1 (7-36)amide and Cholecystokinin-8 in the Endocrine and Exocrine Rat Pancreas

Cited by 34 publications

References 0 publications

Modulation of Acetylcholine-Stimulated Insulin Release by Glucose and Gastric Inhibitory Polypeptide

Modulation of Acetylcholine-Stimulated Insulin Release by Glucose and Gastric Inhibitory Polypeptide

Glucagon‐like peptide‐1(7–36) amide is a new incretin/enterogastrone candidate

Mechanisms of action of glucagon-like peptide 1 in the pancreas

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