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Sodium Channel β1 Regulatory Subunit Deficiency Reduces Pancreatic Islet Glucose-Stimulated Insulin and Glucagon Secretion

By Sara J. Ernst, Lydia Aguilar-Bryan and Jeffrey L. Noebels

Abstract

Glucose-stimulated insulin and glucagon release regulates glucose homeostasis by an excitation-secretion coupling pathway beginning with ATP-sensitive K+ channel closure, membrane depolarization, and entry of calcium ions to stimulate exocytosis. The contribution of voltage-gated sodium channels to this release pathway is still being elucidated. We demonstrate that loss of Scn1b, a major regulatory subunit expressed with Nav1.7 protein in mouse pancreatic islets, reduces glucose-stimulated insulin and glucagon secretion in vitro and in vivo, resulting in severe fed and fasting hypoglycemia. This genetic mouse model is the first to demonstrate that sodium channelopathy impairs the physiological excitation-release coupling pathway for pancreatic insulin and glucagon release

Topics: Article
Publisher: The Endocrine Society
OAI identifier: oai:pubmedcentral.nih.gov:2654754
Provided by: PubMed Central
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