A possible mechanism of the regulation of energy metabolism by mechanical stimulation of skeletal muscle

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K11554
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 59020:Sports sciences-related
• Research Institution: Hirosaki Gakuin University
• Principal Investigator: Munehiro Uda 弘前学院大学, 看護学部, 准教授 (80549262)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 筋萎縮 / ミトコンドリア / 神経型一酸化窒素合成酵素

Outline of Final Research Achievements

Skeletal muscle disuse induces muscle atrophy and insulin resistance that affects energy metabolism. Although both nitric oxide (NO) and nitric oxide synthase (nNOS) may be involved in these changes associated with muscle atrophy, the mechanism remains unclear. We thus investigated the changes in nNOS expression and the proteins that interact with nNOS in hindlimb muscles after unloading. Furthermore, we investigated the alteration of PINK1 and Parkin expression, which are involved in mitochondrial proteolysis. The rats were randomly assigned to control and hindlimb unloading groups. Hindlimb unloading group was exposed to tail suspension for 14 days. Our results suggest that NO production in atrophied muscles may be reduced by hindlimb unloading. In addition, Parkin activity may be downregulated. Therefore, nNOS and its interacting proteins as well as Parkin could be related to the regulation of energy metabolism in the unloaded muscle. But additional studies are required.

Free Research Field

運動生理学

Academic Significance and Societal Importance of the Research Achievements

骨格筋の不活動は筋の萎縮を生じさせるとともに，ミトコンドリアの機能を変化させたり，インスリン抵抗性を生じさせたりして，エネルギー代謝にも影響する。筋萎縮に伴うこれらの変化には一酸化窒素および一酸化窒素合成酵素が関係する可能性が示されているが，そのメカニズムは不明な部分も多い。本研究では骨格筋における神経型一酸化窒素合成酵素とミトコンドリアのタンパク質分解に関わるタンパク質が，筋の不活動時のエネルギー代謝の調節に関係する可能性を検討した。本研究の成果は，筋萎縮のみならず，生活習慣病の治療や予防方法の開発などに貢献することが期待できる。