Open Accessβ‐Cell glutamate signaling: Its role in incretin‐induced insulin secretion
Author(s) -
Yokoi Norihide,
Gheni Ghupurjan,
Takahashi Harumi,
Seino Susumu
Publication year - 2016
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/jdi.12468
Subject(s) - incretin , endocrinology , medicine , secretion , insulin , adenosine , glucose homeostasis , cyclic adenosine monophosphate , signal transduction , diabetes mellitus , type 2 diabetes , insulin resistance , biology , microbiology and biotechnology , receptor
Insulin secretion from the pancreatic β‐cell (referred to as β‐cell hereafter) plays a central role in glucose homeostasis. Impaired insulin secretion is a major factor contributing to the development of diabetes and, therefore, is an important target for treatment of the disease. Cyclic adenosine monophosphate is a key second messenger in β‐cells that amplifies insulin secretion. Incretins released by the gut potentiate insulin secretion through cyclic adenosine monophosphate signaling in β‐cells, which is the basis for the incretin‐based diabetes therapies now being used worldwide. Despite its importance, the interaction between glucose metabolism and incretin/cyclic adenosine monophosphate signaling in β‐cells has long been unknown. A recent study showed that cytosolic glutamate produced by glucose metabolism in β‐cells is a key signal in incretin‐induced insulin secretion. Here we review the physiological and pathophysiological roles of β‐cell glutamate signaling in incretin‐induced insulin secretion.