Pancreatic islets isolated from β2 adrenergic receptor knockout mice show reduced insulin secretion in response to nutrients - doi: 10.4025/actascibiolsci.v35i3.15842

Activation of β2 adrenergic receptors by catecholamine or catecholamine-mimetic substances may enhance insulin secretion. We herein investigated KCl- and nutrient-stimulated insulin secretion in pancreatic islets isolated from β2 knockout (β2KO) mice. β2KO mice showed reduced body weight, fasting hy...

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Bibliographic Details
Authors: Marçal, Anderson Carlos, Davel, Ana Paula Couto, Carpinelli, Angelo Rafael, Brum, Patrícia Chakur, Rossoni, Luciana Venturini, Carvalho, Carla Roberta de Oliveira
Format: article
Status:Published version
Publication Date:2013
Country:Brasil
Institution:Universidade Estadual de Maringá (UEM)
Repository:Acta Scientiarum Biological Sciences
Language:Portuguese
English
OAI Identifier:oai:periodicos.uem.br/ojs:article/15842
Online Access:http://www.periodicos.uem.br/ojs/index.php/ActaSciBiolSci/article/view/15842
Access Level:Open access
Keyword:adrenergic receptors
pancreatic beta cells
glucose
leucine
(Citologia e Biologia Celular)
(Fisiologia de órgãos e sistemas).
Description
Summary:Activation of β2 adrenergic receptors by catecholamine or catecholamine-mimetic substances may enhance insulin secretion. We herein investigated KCl- and nutrient-stimulated insulin secretion in pancreatic islets isolated from β2 knockout (β2KO) mice. β2KO mice showed reduced body weight, fasting hypoglycaemia associate to a similar fasting insulinemia compared to control. β2KO mice also showed reduced glucose tolerance despite the higher sensitivity to insulin. Glucose-induced insulin secretion was impaired in pancreatic islets isolated from β2KO mice. Leucine-induced (20mM) insulin secretion was diminished in pancreatic islets isolated from β2KO mice when compared to control one. The depolarizing effect of KCl on insulin secretion was also impaired in pancreatic islets from β2KO mice. These results suggested a possible role of β2 adrenergic receptors on nutrient-induced insulin secretion.