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

• Autor(a) principal: Marçal, Anderson Carlos
• Data de Publicação: 2013
• Outros Autores: Davel, Ana Paula Couto, Carpinelli, Angelo Rafael, Brum, Patrícia Chakur, Rossoni, Luciana Venturini, Carvalho, Carla Roberta de Oliveira
• Tipo de documento: Artigo
• Idioma: por; eng
• Título da fonte: Acta Scientiarum Biological Sciences
• Texto Completo: http://www.periodicos.uem.br/ojs/index.php/ActaSciBiolSci/article/view/15842
• topic: adrenergic receptors; pancreatic beta cells; glucose; leucine; (Citologia e Biologia Celular); (Fisiologia de órgãos e sistemas).

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.