| Project/Area Number |
17K16145
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | University of Yamanashi |
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Principal Investigator |
Masashi ICHIJO 山梨大学, 大学院総合研究部, 助教 (50436854)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 糖尿病 / 膵β細胞 / インスリン分泌 / β細胞 / インスリン / プロスタシン |
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| Outline of Final Research Achievements |
In pancreatic beta cell-specific prostasin KO mice (β KO), we found in our studies that blood glucose levels were significantly higher in the glucose tolerance test.In MIN6 in which prostasin was knocked down, Ca2+ uptake was reduced at high glucose concentration.Immunoelectron microscopic examination of mouse pancreatic β cells revealed that prostasin was expressed in the form of insulin secretory granules.From the above, it is strongly suggested by this study that prostasin plays an important role in insulin secretion in pancreatic β cells.
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| Academic Significance and Societal Importance of the Research Achievements |
膵β細胞におけるインスリン分泌において、プロスタシンが重要な役割を働いていることが本研究により示唆された。インスリン分泌に関わる新たなメカニズムの発見であり、本研究結果が糖尿病に関する新たな病態の解明や、新規薬剤の開発に寄与する可能性がある。
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