Self-inducible secretion of glucagon-like peptide-1 (GLP-1) that allows MIN6 cells to maintain insulin secretion and insure cell survival

2012 ◽  
Vol 349 (2) ◽  
pp. 281-288 ◽  
Author(s):  
Koji Nakashima ◽  
Masashi Shimoda ◽  
Sumiko Hamamoto ◽  
Fuminori Tatsumi ◽  
Hidenori Hirukawa ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Survival ◽  
Min6 Cells ◽  
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 Subthreshold α2-Adrenergic Activation Counteracts Glucagon-Like Peptide-1 Potentiation of Glucose-Stimulated Insulin Secretion

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Minglin Pan ◽  
Guang Yang ◽  
Xiuli Cui ◽  
Shao-Nian Yang
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Adrenergic Agonist ◽  
Signaling Systems ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
Insulin Secretory Response ◽  
Adrenergic Activation ◽  
Gi Proteins

The pancreatic β cell harbors α2-adrenergic and glucagon-like peptide-1 (GLP-1) receptors on its plasma membrane to sense the corresponding ligands adrenaline/noradrenaline and GLP-1 to govern glucose-stimulated insulin secretion. However, it is not known whether these two signaling systems interact to gain the adequate and timely control of insulin release in response to glucose. The present work shows that the α2-adrenergic agonist clonidine concentration-dependently depresses glucose-stimulated insulin secretion from INS-1 cells. On the contrary, GLP-1 concentration-dependently potentiates insulin secretory response to glucose. Importantly, the present work reveals that subthreshold α2-adrenergic activation with clonidine counteracts GLP-1 potentiation of glucose-induced insulin secretion. This counteractory process relies on pertussis toxin- (PTX-) sensitive Gi proteins since it no longer occurs following PTX-mediated inactivation of Gi proteins. The counteraction of GLP-1 potentiation of glucose-stimulated insulin secretion by subthreshold α2-adrenergic activation is likely to serve as a molecular mechanism for the delicate regulation of insulin release.

Differential Importance of Glucose-Dependent Insulinotropic Polypeptide vs Glucagon-Like Peptide 1 Receptor Signaling for Beta Cell Survival in Mice

2009 ◽  
Vol 137 (6) ◽  
pp. 2146-2157 ◽  
Author(s):  
Adriano Maida ◽  
Tanya Hansotia ◽  
Christine Longuet ◽  
Yutaka Seino ◽  
Daniel J. Drucker
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1
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