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2015 Fiscal Year Final Research Report

Potentiation of Glucose-Stimulated Insulin Secretion by GPR40-PLC-TRPC Pathway and cAMP-EPAC2-TRPM2 Pathway in Pancreatic Beta Cells

Research Project

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Project/Area Number 26870532
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Endocrinology
Metabolomics
Research InstitutionJichi Medical University

Principal Investigator

Yoshida Masashi  自治医科大学, 医学部, 助教 (50528411)

Project Period (FY) 2014-04-01 – 2016-03-31
Keywords膵β細胞 / インクレチン / GPR40 / GLP-1 / Trpm2 / TrpC3
Outline of Final Research Achievements

It has been proposed that glucose-stimulated insulin secretion is initiated by closure of KATP channels, followed by membrane depolarization. In theory, however, closure of KATP channels is insufficient to shift the membrane potential toward a threshold level, since membrane potential is determined by the overall balance between outward and inward currents. Modest constitutional opening of background inward current through nonselective cation channels (NSCCs) is crucial to facilitate depolarization. Recently, we demonstrated that a class of NSCC is activated by both glucose metabolism and incretin hormones, via Trpm2 pathway. In this study, we demonstrate that gastric hormone ghrelin attenuates glucose-induced insulin secretion via TRPM2 pathway. We also demonstrate that GPR40 agonist stimulate insulin secretion via the TRPC3 channel pathway. We believe that TRPM2 pathway and TRPC3 pathway provide a potential therapeutic target for the treatment of type 2 diabetes.

Free Research Field

インスリン分泌

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Published: 2017-05-10  

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