| Project/Area Number |
15K09388
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
片上 直人 大阪大学, 医学系研究科, 寄附講座講師 (10403049)
河盛 段 大阪大学, 医学系研究科, 助教 (50622362)
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 糖尿病 / 高血糖毒性 / 膵β細胞障害 / 膵β細胞再生 / 膵β細胞糖毒性 / インスリン分泌 / インスリン転写因子 / 分化転換 / ｲﾝｽﾘﾝ転写因子 / 膵β細胞 |
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| Outline of Final Research Achievements |
The dysfunction of pancreatic beta cells results in hyperglycemia, which causes further dysfunction of beta cells. And, that leads progressed diabetes. Our purpose in this study is to clarify how hyperglycemia impairs beta cells. We newly identified the beta-cell factor, which is fragile to chronic high glucose, and indicated that that is critical for insulin secretion using the knock-out mouse model.
Another objectives is to find candidate cells to be capable of transdifferentiation to pancreatic beta cells in vivo. First of all, we generated transgenic mice to conditionally express transcription factors which are critical for beta-cell differentiation. Using those, we found pancreatic non-beta cells are the candidate for the transdifferentiation into beta cells.
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