| Project/Area Number |
15K12705
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied health science
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| Research Institution | University of Shizuoka |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
金子 雪子 静岡県立大学, 薬学部, 講師 (00381038)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| 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 / セロトニン / メラトニン |
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| 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.
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