| Project/Area Number |
17K09830
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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 |
Junji Kozawa 大阪大学, 医学系研究科, 寄附講座准教授 (80513001)
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| Co-Investigator(Kenkyū-buntansha) |
岩橋 博見 大阪大学, 医学系研究科, 寄附講座准教授 (60397627)
福井 健司 大阪大学, 医学系研究科, 助教 (60513009)
木村 武量 大阪大学, 医学系研究科, 助教 (70770171)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 膵β細胞 / 膵α細胞 / 分化転換 / 再生療法 / 糖尿病 / 膵脂肪化 / 耐糖能異常 / 膵島構造異常 / ARX / 脱分化 |
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| Outline of Final Research Achievements |
In pancreatic histological analyses in patients who underwent pancreatectomy in Osaka university hospital, pancreatic alpha-cell proliferation and the area ratio of alpha cell/beta cell increased in patients with long-standing type 2 diabetes. The reduced beta-cell mass was associated with the reduced expression of ARX and the increased expression of NKX6.1 in alpha cell. This suggested that the compensation for the reduced beta-cell mass through proliferation and transdifferentiation of alpha cell. In addition, the progression of diabetes intolerance was associated with pancreatic fatty infiltration and islet inflammation.
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| Academic Significance and Societal Importance of the Research Achievements |
本邦において、糖尿病患者は増加の一途を辿り、糖尿病治療薬の開発は進んでいるが、未だ膵β細胞量の減少に対する根治的な治療法は開発されていない。膵α細胞のARXを中心とする転写因子発現変化が膵β細胞への分化転換へつながる可能性、今後の膵α細胞におけるARX発現調節を介した膵β細胞再生療法への組織学的な基盤が示された。
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