Inhibitory Action of Islet Amyloid Polypeptide and Calcitonin Gene-related Peptide on Release of Insulin from the Isolated Perfused Rat Pancreas

Kogire, Masafumi; Ishizuka, Jin; Thompson, James C.; Greeley, George H.

doi:10.1097/00006676-199107000-00013

Cited by 59 publications

(27 citation statements)

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“…Amylin, first isolated from amyloid deposits of insulinoma and type 2 diabetes pancreas (67) in late 1980s, shares 43% and 46% homology with α-CGRP and β-CGRP, respectively (68). Evidence from numerous pre-clinical studies shows that (28,(69)(70)(71)(72)(73), whereas amylin acts to reduce glucose-stimulated insulin release in non-insulin dependent diabetic rat islets, increased amylin causes peripheral insulin resistance possibly by acting directly on insulin secretion within the islet. Although the authors of aforementioned studies suggest that CGRP likely impairs insulin secretion and induces insulin resistance in the same manner as amylin (28,(69)(70)(71)(72)(73) in non-insulin dependent diabetes, our findings suggest that CGRP may be involved in glucose homeostasis only in the absence or non-functionality of amylin.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence from numerous pre-clinical studies shows that (28,(69)(70)(71)(72)(73), whereas amylin acts to reduce glucose-stimulated insulin release in non-insulin dependent diabetic rat islets, increased amylin causes peripheral insulin resistance possibly by acting directly on insulin secretion within the islet. Although the authors of aforementioned studies suggest that CGRP likely impairs insulin secretion and induces insulin resistance in the same manner as amylin (28,(69)(70)(71)(72)(73) in non-insulin dependent diabetes, our findings suggest that CGRP may be involved in glucose homeostasis only in the absence or non-functionality of amylin. This is supported by recent evidence that shows amylin levels are elevated in patients with abnormal glucose metabolism after acute pancreatitis (20,21), and are significantly associated with pro-inflammatory cytokines, in particular interleukin-6 and monocyte chemoattractant protein-1 (21).…”

Section: Discussionmentioning

confidence: 99%

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Calcitonin gene-related peptide: neuroendocrine communication between the pancreas, gut, and brain in regulation of blood glucose

et al. 2017

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Background: Calcitonin gene-related peptide (CGRP), a ubiquitous neuropeptide, plays a diverse and intricate role in chronic low-grade inflammation, including conditions such as obesity, type 2 diabetes, and diabetes of the exocrine pancreas. Diabetes of exocrine pancreas is characterised by chronic hyperglycemia and is associated with persistent low-grade inflammation and altered secretion of certain pancreatic and gut hormones. While CGRP may regulate glucose homeostasis and the secretion of pancreatic and gut hormones, its role in chronic hyperglycemia after acute pancreatitis (CHAP) is not known. The aim of this study was to investigate the association between CGRP and CHAP.Methods: Fasting blood samples were collected to measure insulin, HbA1c, CGRP, amylin, C-peptide, glucagon, pancreatic polypeptide (PP), somatostatin, gastric inhibitory peptide, glicentin, glucagon-like peptide-1 and 2, and oxyntomodulin. Modified Poisson regression analysis and linear regression analyses were conducted. Five statistical models were used to adjust for demographic, metabolic, and pancreatitisrelated risk factors.Results: A total of 83 patients were recruited. CGRP was significantly associated with CHAP in all five models (P-trend <0.005). Further, it was significantly associated with oxyntomodulin (P<0.005) and glucagon (P<0.030). Oxyntomodulin and glucagon independently contributed 9.7% and 7%, respectively, to circulating CGRP variance. Other pancreatic and gut hormones were not significantly associated with CGRP.Conclusions: CGRP is involved in regulation of blood glucose in individuals after acute pancreatitis. This may have translational implications in prevention and treatment of diabetes of the exocrine pancreas.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Calcitonin gene-related peptide: neuroendocrine communication between the pancreas, gut, and brain in regulation of blood glucose

et al. 2017

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“…In pancreatic islets, CGRP was reported to inhibit insulin release (Kogire et al, 1991). Conversely, after glucose challenge, attenuated insulin secretion was noted in the SP-deficient mice.…”

Section: E Transient Receptor Potential Channels In Obesity and Metamentioning

confidence: 99%

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

2014

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“…Recently, amylin has been shown to inhibit glucose-induced insulin output in different in vitro systems, such as the rat perfused pancreas Silvestre et al, 1993), rat perifused islets (Wang et al, 1993), and mouse isolated fl-cells (Wagoner et al, 1993). In the perfused pancreas of the rat, short-term infusion of amylin has shown that amylin inhibits the insulin response to secretagogues that act on the f-cell via different mechanisms namely, K and Ca channels, the adenylate cyclase/cyclic AMP system, and phospholipid turnover (Kogire et al, 1991;Salas et al, 1993;Silvestre et al, 1994). It should be emphasized that such an effect has been observed with an amylin concentration (75 pM) comparable to amylin levels found in the effluent of the rat perfused pancreas Silvestre et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Effect of (8–32) salmon calcitonin, an amylin antagonist, on insulin, glucagon and somatostatin release: study in the perfused pancreas of the rat

Silvestre

Salas²,

Rodriguez-Gallardo³

et al. 1996

British J Pharmacology

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1 The 8 -32 fragment of salmon calcitonin ((8 -32) sCT) has been proposed as a highly selective amylin receptor antagonist. 2 In the present study, we have studied the influence of (8-32) sCT on the inhibitory effect of both amylin and its structural congener, calcitonin gene-related peptide (CGRP), on insulin secretion in the rat perfused pancreas. 3 Both amylin and CGRP, at 75 pM, clearly inhibited glucose-induced insulin release (by 80% and by 70%, respectively). Simultaneous infusion of 10 [gM (8-32) sCT reversed the inhibitory effect of amylin (by 80%; P<0.05 vs. amylin experiments) but did not significantly affect the inhibition of glucoseinduced insulin output elicited by CGRP. Furthermore, at the same concentration (10 giM), sCT alone potentiated the insulin response to 7 mM glucose (2.5 fold; P<0.05) whilst it did not affect glucagon or somatostatin secretion. 4 The observation that infusion of an amylin antagonist into the rat pancreas potentiates the insulin response to glucose, favours the concept of endogenous amylin as an inhibitor of insulin release. 5Finally, as an amylin antagonist at the level of the fl-cell, (8-32) sCT might be considered of potential interest in experimental and clinical pharmacology.

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Inhibitory Action of Islet Amyloid Polypeptide and Calcitonin Gene-related Peptide on Release of Insulin from the Isolated Perfused Rat Pancreas

Cited by 59 publications

References 0 publications

Calcitonin gene-related peptide: neuroendocrine communication between the pancreas, gut, and brain in regulation of blood glucose

Calcitonin gene-related peptide: neuroendocrine communication between the pancreas, gut, and brain in regulation of blood glucose

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

Effect of (8–32) salmon calcitonin, an amylin antagonist, on insulin, glucagon and somatostatin release: study in the perfused pancreas of the rat

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