| Project/Area Number |
15K19527
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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 | Juntendo University |
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Principal Investigator |
komiya koji 順天堂大学, 医学部, 助教 (50385077)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 糖尿病 / オートファジー / バイオマーカー / Rubicon / 膵β細胞障害 / プロテアソームアルファサブユニット6 |
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| Outline of Final Research Achievements |
We reported that the insufficiency of Autophagy (AP) impaired beta-cell functions. The purpose of this study is to identify the marker for monitoring AP in vivo. Moreover, this study examines that the AP’s function enhanced by the suppression of Rubicon (Rb), AP inhibitor, improves beta-cell function.
We detected proteasome subunit (PMS) in the culture medium of AP deficient beta-cell lines. In addition, we recognized an increase in the amount of PMS in the serum of beta-cell specific AP deficient mice. The results suggest that PMS is one of the markers for monitoring AP in vivo. From now on, the investigation of the specificity will be needed.
To suppress Rb did not enhance the function of AP in a steady-state beta-cell lines or mice. Looking ahead, we will verify it in an AP failure conditions.
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