| Project/Area Number |
16H05157
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
八木下 尚子 聖マリアンナ医科大学, 医学研究科, 講師 (40367389)
荒谷 聡子 東京医科大学, 医学部, 講師 (40387064)
藤田 英俊 東京医科大学, 医学部, 講師 (90571802)
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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 |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2018: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2016: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
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| Keywords | サルコペニア / 遺伝子改変動物 / タンパク質分解 / シノビオリン / ユビキチン化 |
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| Outline of Final Research Achievements |
We have been studying the role of synoviolin in several energy metabolism organs including white adipose tissue and liver. In this study, we focused on the role of synoviolin in skeletal muscle which is one of the representative energy metabolizing organs. The muscle-specific synoviolin knockout mice showed the severe muscle atrophy at 6 weeks of birth. In addition, pathological and physiological analyses demonstrated that the muscle atrophy mainly occurred in fast muscle fibers and muscle strength was also reduced.
These results reinforce our previous finding that synoviolin plays a pivotal key regulator of energy metabolism. Taken together, this study could provide the new model to investigate muscle atrophy including sarcopenia.
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| Academic Significance and Societal Importance of the Research Achievements |
超高齢化社会を迎えた日本では運動器の障害により日常生活に支援や介護が必要となる方が増加している。平均余命が延びている分だけ、運動器の健康を長く保つ必要があり、サルコペニアの病態研究は国民にとって喫緊の最重要課題の一つである（「健康日本21」より）。しかし、「加齢」という生命現象自体が未だ謎の点が多く、期間、その他の要因など問題がある。本研究によりこれらを解決した迅速に得られる新規筋萎縮モデルを提供でき、本分野の研究の発展に寄与できよう。
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