| Project/Area Number |
16K08520
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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 |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | Chiba University |
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Principal Investigator |
MIKI Takashi 千葉大学, 大学院医学研究院, 教授 (50302568)
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| Co-Investigator(Kenkyū-buntansha) |
李 恩瑛 千葉大学, 大学院医学研究院, 助教 (60583424)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 糖尿病 / 膵β細胞 / 再生医学 / インスリン / 糖 / 栄養学 / 生理学 |
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| Outline of Final Research Achievements |
Deterioration of pancreatic islets in terms of their quantity and quality is the major cause for developing diabetes mellitus. To clarify its pathophysiology, we have established two lines of mouse models; islet regeneration mice and pseudoislet-transplanted mice. Islet regeneration mice were generated so as to express diphtheria toxin receptor specifically in pancreatic β-cells, whereas pseudoislet-transplanted mice were generated by transplanting pseudoislets made from pancreatic β-cell line MIN6 cells. Analyses of islet regeneration mice revealed that highly proliferative cells appeared in the islet after pancreatic β-cell depletion. In the pseudoislet-transplanted mice, pancreatic β-cells exhibited increased apoptosis and de-differentiation in the face of excessive exogenous pancreatic β-cells. These results indicated that quantity and quality of pancreatic β-cells is maintained through elaborate sensing of the demand of pancreatic β-cells in vivo.
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| Academic Significance and Societal Importance of the Research Achievements |
糖尿病では、膵島量減少が発症に先行して出現し、発症後も進行する。しかし、現行の糖尿病治療薬では膵島の量と質の回復は期待できない。一方、もし膵島量の減少阻止や回復が可能になれば、これらが糖尿病の根治治療になる可能性がある。このような糖尿病の生成治療の確立には、膵島量の制御機構の解明が不可欠である。本研究により解明された膵島量調節機構は、将来の膵島再生による糖尿病治療法の確立に向けた学術的な基盤を与えるものであると考えている。
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