| Project/Area Number |
17K01765
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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 |
Sports science
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
関根 紀子 順天堂大学, スポーツ健康科学部, 客員准教授 (10393175)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 骨格筋萎縮 / ヒストン脱アセチル化酵素 / サルコペニア / ヒストン修飾 / エピジェネティクス / マッスルメモリー / 運動習慣 / 不活動習慣 / 若年期 |
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| Outline of Final Research Achievements |
This study investigated the hypothesis that physical inactivity in adolescents affects subsequent hindlimb unloading-induced muscle atrophy in rat soleus muscle. Long-term physical inactivity in adolescents did not alter the metabolic and physiological characteristics of growing rats. However, the decline in the soleus muscle weight induced by 7 days of hindlimb unloading was drastic in the physically inactive group. This may be due to the physical inactivity-induced upregulation of histone deacetylase 4 (HDAC4) and downstream gene expression. Furthermore, we also investigated age-related differences in the activation of the HDAC4/Gadd45α pathway following hindlimb unloading. We found that levels of HDAC4 and Gadd45αprotein and mRNA were significantly increased in the old age group. These data suggest that countermeasures targeting HDAC4 may be effective in suppressing muscle atrophy due to physical inactivity and aging.
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| Academic Significance and Societal Importance of the Research Achievements |
近年，ヒトの疾患を引き起こす原因として，遺伝的な異常のみならず，環境的な因子によるエピジェネティクスの異常が注目されており，特に若年期の生育環境や栄養はその後の肥満症や生活習慣病の罹患リスクに多大な影響を与える可能性が示されつつある。若年期の運動不足は，その後の筋の不適応，すなわち筋萎縮の生じやすさに悪影響を与えるという本研究の成果は、若年期における運動不足のリスクを示唆するものである。このような分子機序の解明は、運動不足に関連した多くの多因子疾患の進行に歯止めをかけるための第一歩となり，多因子疾患に対する新たな医学的アプローチ，運動効果模倣薬の開発などあらゆる分野への貢献が期待される。
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