scholarly journals Generation of Nicotinic Acid Adenine Dinucleotide Phosphate and Cyclic ADP-Ribose by Glucagon-Like Peptide-1 Evokes Ca2+ Signal That Is Essential for Insulin Secretion in Mouse Pancreatic Islets

Diabetes ◽  
2008 ◽  
Vol 57 (4) ◽  
pp. 868-878 ◽  
Author(s):  
B.-J. Kim ◽  
K.-H. Park ◽  
C.-Y. Yim ◽  
S. Takasawa ◽  
H. Okamoto ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Nicotinic Acid ◽  
Pancreatic Islets ◽  
Cyclic Adp Ribose ◽  
Mouse Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The Effect of Zinc-Crystallized Glucagon-Like Peptide-1 on Insulin Secretion of Macroencapsulated Pancreatic Islets

2001 ◽  
Vol 7 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Heather Gappa ◽  
Miroslav Baudyš ◽  
Jae Joon Koh ◽  
Sung Wan Kim ◽  
You Han Bae
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Insulin secretion defects in liver cirrhosis can be reversed by glucagon-like peptide-1

2000 ◽  
Vol 164 (1) ◽  
pp. 13-19 ◽  
Author(s):  
EG Siegel ◽  
A Seidenstucker ◽  
B Gallwitz ◽  
F Schmitz ◽  
A Reinecke-Luthge ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Liver Cirrhosis ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Dependent Manner ◽  
Isolated Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Liver cirrhosis is often accompanied by a disturbed carbohydrate metabolism similar to type 2 diabetes. To investigate the severity of the defect in insulin secretion in this form of diabetes, we measured insulin release from isolated pancreatic islets of rats with CCl(4)-phenobarbital-induced liver cirrhosis. Cirrhosis was confirmed by clinical signs, elevated liver enzymes and histology. Fasting venous plasma glucose concentrations were equal in rats with liver cirrhosis and in controls. Plasma insulin and glucagon concentrations were significantly greater (P<0.01) in cirrhotic rats than in control animals. Glucose (16.7 mM)-induced stimulation of insulin release from pancreatic islets revealed a twofold increase in control and cirrhotic rats. Basal and stimulated insulin secretion, however, were significantly lower in cirrhotic animals. The incretin hormone, glucagon-like peptide-1 (GLP-1), has therapeutic potential for the treatment of type 2 diabetes. Therefore, islets from control and cirrhotic animals were incubated with GLP-1 in concentrations from 10(-)(11) to 10(-)(6) M. GLP-1 stimulated insulin release in a concentration-dependent manner. In islets from cirrhotic rats, basal and stimulated insulin secretion was blunted compared with controls. These data show that the hyperinsulinemia observed in liver cirrhosis is not due to an increase of insulin secretion from islets, but could be explained by decreased hepatic clearance of insulin. GLP-1 may ameliorate diabetes in patients with liver cirrhosis.

Altered cAMP and Ca2+ signaling in mouse pancreatic islets with glucagon-like peptide-1 receptor null phenotype

Diabetes ◽  
1999 ◽  
Vol 48 (10) ◽  
pp. 1979-1986 ◽  
Author(s):  
D. Flamez ◽  
P. Gilon ◽  
K. Moens ◽  
A. Van Breusegem ◽  
D. Delmeire ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Null Phenotype ◽  
Mouse Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet

2013 ◽  
Vol 27 (8) ◽  
pp. 1198-1207 ◽  
Author(s):  
Alessandro Ustione ◽  
David W. Piston ◽  
Paul E. Harris
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Dopaminergic Neurons ◽  
Feedback Loop ◽  
Β Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
Dopaminergic Regulation ◽  
Physiologic Role

Exogenous dopamine inhibits insulin secretion from pancreatic β-cells, but the lack of dopaminergic neurons in pancreatic islets has led to controversy regarding the importance of this effect. Recent data, however, suggest a plausible physiologic role for dopamine in the regulation of insulin secretion. We review the literature underlying our current understanding of dopaminergic signaling that can down-regulate glucose-stimulated insulin secretion from pancreatic islets. In this negative feedback loop, dopamine is synthesized in the β-cells from circulating l-dopa, serves as an autocrine signal that is cosecreted with insulin, and causes a tonic inhibition on glucose-stimulated insulin secretion. On the whole animal scale, l-dopa is produced by cells in the gastrointestinal tract, and its concentration in the blood plasma increases following a mixed meal. By reviewing the outcome of certain types of bariatric surgery that result in rapid amelioration of glucose tolerance, we hypothesize that dopamine serves as an “antiincretin” signal that counterbalances the stimulatory effect of glucagon-like peptide 1.

scholarly journals Equine glucagon-like peptide-1 receptor physiology

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4316 ◽  
Author(s):  
Murad H. Kheder ◽  
Simon R. Bailey ◽  
Kevin J. Dudley ◽  
Martin N. Sillence ◽  
Melody A. de Laat
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Insulin Response ◽  
Synthetic Analogue ◽  
Isolated Pancreatic Islets ◽  
Novel Approach ◽  
Insulin Dysregulation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Background Equine metabolic syndrome (EMS) is associated with insulin dysregulation, which often manifests as post-prandial hyperinsulinemia. Circulating concentrations of the incretin hormone, glucagon-like peptide-1 (GLP-1) correlate with an increased insulin response to carbohydrate intake in animals with EMS. However, little is known about the equine GLP-1 receptor (eGLP-1R), or whether GLP-1 concentrations can be manipulated. The objectives were to determine (1) the tissue localisation of the eGLP-1R, (2) the GLP-1 secretory capacity of equine intestine in response to glucose and (3) whether GLP-1 stimulated insulin secretion from isolated pancreatic islets can be attenuated. Methods Archived and abattoir-sourced tissues from healthy horses were used. Reverse transcriptase PCR was used to determine the tissue distribution of the eGLP-1R gene, with immunohistochemical confirmation of its pancreatic location. The GLP-1 secretion from intestinal explants in response to 4 and 12 mM glucose was quantified in vitro. Pancreatic islets were freshly isolated to assess the insulin secretory response to GLP-1 agonism and antagonism in vitro, using concentration-response experiments. Results The eGLP-1R gene is widely distributed in horses (pancreas, heart, liver, kidney, duodenum, digital lamellae, tongue and gluteal skeletal muscle). Within the pancreas the eGLP-1R was immunolocalised to the pancreatic islets. Insulin secretion from pancreatic islets was concentration-dependent with human GLP-1, but not the synthetic analogue exendin-4. The GLP-1R antagonist exendin 9-39 (1 nM) reduced (P = 0.08) insulin secretion by 27%. Discussion The distribution of the eGLP-1R across a range of tissues indicates that it may have functions beyond insulin release. The ability to reduce insulin secretion, and therefore hyperinsulinemia, through eGLP-1R antagonism is a promising and novel approach to managing equine insulin dysregulation.

scholarly journals Exendin-(9–39) Is an Inverse Agonist of the Murine Glucagon-Like Peptide-1 Receptor: Implications for Basal Intracellular Cyclic Adenosine 3′,5′-Monophosphate Levels and β-Cell Glucose Competence**This work was supported by Grant 31-46958.96 from the Swiss National Science Foundation (to B.T.).

Endocrinology ◽  
1998 ◽  
Vol 139 (11) ◽  
pp. 4448-4454 ◽  
Author(s):  
Véronique Serre ◽  
Wanda Dolci ◽  
Elizabeth Schaerer ◽  
Louise Scrocchi ◽  
Daniel Drucker ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Messenger Rna ◽  
Inverse Agonist ◽  
Intracellular Camp ◽  
Endogenous Production ◽  
Mouse Pancreatic Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
Camp Levels

Abstract The effect of exendin-(9–39), a described antagonist of the glucagon-like peptide-1 (GLP-1) receptor, was evaluated on the formation of cAMP- and glucose-stimulated insulin secretion (GSIS) by the conditionally immortalized murine βTC-Tet cells. These cells have a basal intracellular cAMP level that can be increased by GLP-1 with an EC50 of approximately 1 nm and can be decreased dose dependently by exendin-(9–39). This latter effect was receptor dependent, as aβ -cell line not expressing the GLP-1 receptor was not affected by exendin-(9–39). It was also not due to the endogenous production of GLP-1, because this effect was observed in the absence of detectable preproglucagon messenger RNA levels and radioimmunoassayable GLP-1. Importantly, GSIS was shown to be sensitive to this basal level of cAMP, as perifusion of βTC-Tet cells in the presence of exendin-(9–39) strongly reduced insulin secretion. This reduction of GSIS, however, was observed only with growth-arrested, not proliferating, βTC-Tet cells; it was also seen with nontransformed mouse β-cells perifused in similar conditions. These data therefore demonstrated that 1) exendin-(9–39) is an inverse agonist of the murine GLP-1 receptor; 2) the decreased basal cAMP levels induced by this peptide inhibit the secretory response of βTC-Tet cells and mouse pancreatic islets to glucose; 3) as this effect was observed only with growth-arrested cells, this indicates that the mechanism by which cAMP leads to potentiation of insulin secretion is different in proliferating and growth-arrested cells; and 4) the presence of the GLP-1 receptor, even in the absence of bound peptide, is important for maintaining elevated intracellular cAMP levels and, therefore, the glucose competence of theβ -cells.

Stimulation of Insulin Secretion by a Novel Small Molecule Glucagon-Like Peptide-1 Receptor Agonist in Rodent and Human Islets.

2010 ◽  
pp. P1-479-P1-479
Author(s):  
KW Sloop ◽  
FS Willard ◽  
MB Brenner ◽  
J Ficorilli ◽  
K Valasek ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Small Molecule ◽  
Receptor Agonist ◽  
Human Islets ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Stimulation Of
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