Insight into mechanisms of insulin secretion induced by KATP-independent action and incretin

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461383
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: Shinshu University
• Principal Investigator: KOMATSU Mitsuhisa 信州大学, 学術研究院医学系, 教授 (90221978)
• Co-Investigator(Kenkyū-buntansha): SUZUKI Satoru 福島県立医科大学, 医学部, 教授 (30222061) ; NISHIO Shin-ichi 信州大学, 学術研究院医学系(医学部附属病院), 講師 (30467146)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: インスリン分泌

Outline of Final Research Achievements

In search of mechanisms of glucose-stimulates insulin secretion, we established two different aspects of findings as follows.
1)We demonstrated that glucose could trigger rapid insulin release independent from its action on both KATP channel and voltage-dependent Ca2+ channel. Namely, with diazoxide, an opener of KATP channel, and nifedipine, a blocker of L-type voltage-dependent Ca2+ channel, glucose triggered insulin secretion from rat pancreatic islets in the presence of forskolin, an activator of adenylyl cyclase. 2)Lactisole, an inhibitor of sweet taste receptor, inhibited insulin secretion induced by sweeteners. It attenuated the elevation of cytoplasmic Ca2+ concentrations induced by these sweeteners. It also inhibited action of glucose. These results indicate that lactisole may be useful in assessing the role of the glucose-sensing receptor in pancreatic β-cells.

Free Research Field

糖尿病学、内分泌学