Idenitification of the endogenous ligand for the sweet taste receptor expressed in pancreatic beta-cells

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670431
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Metabolomics
• Research Institution: Gunma University
• Principal Investigator: KOJIMA Itaru 群馬大学, 生体調節研究所, 教授 (60143492)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 甘味受容体 / 膵β細胞 / インスリン分泌 / グルコース

Outline of Final Research Achievements

The purpose of this study was to identify an endogenous ligand for the sweet taste receptor expressed in pancreatic beta-cells and adipocytes. We initially searched for intracellular compounds which activate the receptor. During the course of the study, we found that glucose is an endogenous ligand for this receptor. We therefore designated this receptor "the glucose-sensing receptor". We investigated the function and physiological role of this receptor in the action of glucose in beta-cells. We found that glucose activates the receptor, facilitates the metabolism in mitochondria and enhances the production of ATP. Since blockade of the receptor results in reduction of insulin secretion, we conclude that glucose-sensing receptor is involved in the action of glucose on insulin secretion. We also studied the changes in the expression of the glucose-sensing receptor in pancreatic beta-cells. The expression of the receptor is markedly reduced after the meal and hyperglycemia.

Free Research Field

内分泌代謝学