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2017 Fiscal Year Final Research Report

Possible involvement of gut-derived melatonin as a negative regulator of insulin secretion

Research Project

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Project/Area Number 15K12705
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Applied health science
Research InstitutionUniversity of Shizuoka

Principal Investigator

Ishikawa Tomohisa  静岡県立大学, 薬学部, 教授 (10201914)

Co-Investigator(Kenkyū-buntansha) 金子 雪子  静岡県立大学, 薬学部, 講師 (00381038)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords膵β細胞 / インスリン分泌 / メラトニン受容体 / N-アセチルセロトニン
Outline of Final Research Achievements

Melatonin derives from serotonin via N-acetylserotonin (NAS). The expression of melatonin receptors in pancreatic β-cells has been demonstrated; however, physiological roles of melatonin receptors or their intrinsic ligands in β-cells remain to be fully elucidated. In this study, we found that AANAT, which converts serotonin to NAS, is expressed in pancreatic β-cells, suggesting that NAS is produced from serotonin in β-cells. We therefore tested the hypothesis that NAS functions as autocrine in β-cells. We showed that NAS inhibits glucose-induced [Ca2+]i oscillation and insulin secretion in β-cells through the activation of melatonin MT2 receptors, and that the expression of AANAT is significantly decreased in pancreatic islets at gestational day 12. These results suggest that NAS produced in β-cells functions as autocrine, inhibiting insulin secretion via MT2 receptors, and that this mechanism may contribute to the regulation of blood glucose during gestational period.

Free Research Field

Pharmacology

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Published: 2019-03-29  

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