Novel mechanism of muscle atrophy mediated by glucose receptors

2022 Fiscal Year Final Research Report

• Project/Area Number: 21K19726
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
• Research Institution: Tokyo Metropolitan University
• Principal Investigator: Furuichi Yasuro 東京都立大学, 人間健康科学研究科, 助教 (40733035)
• Project Period (FY): 2021-07-09 – 2023-03-31
• Keywords: 筋萎縮 / 筋再生 / 受容体 / 代謝変化 / 筋芽細胞

Outline of Final Research Achievements

We searched for new factors associated with skeletal muscle atrophy and discovered that there is an increase in receptors of unknown function during this process. To better understand the molecular function of these receptors, we performed experiments using mouse skeletal muscle stem cells, where we inhibited the expression of receptors using siRNA. The results showed that cell proliferation was promoted and that these receptors had a negative effect on the proliferative ability of muscle cells. We also performed comprehensive gene expression analysis and simultaneous quantitative analysis of metabolites in the same experimental system to elucidate the signaling mechanism of cell proliferation regulated by the receptor. Although the receptor was previously known to induce inflammatory responses in other tissues, our research revealed a novel pathway involved in myocyte proliferation that is distinct from the previously known pathway.

Free Research Field

運動生化学

Academic Significance and Societal Importance of the Research Achievements

加齢や不活動による骨格筋の萎縮は、運動能力を低下させて生活の質を落とすだけでなく、種々の疾患を誘因するため、筋萎縮の原因を解明し、具体的な対抗策を講じることが求められている。筋幹細胞の増殖力を低下させる受容体の発見とその機能解析は、筋萎縮の新たな機序の解明につながる。特に受容体の場合は、拮抗する化合物が発見されれば、運動を模倣するような新薬や食品化合物の発見に結びつき、その波及効果は大きい。本研究では、筋萎縮を誘導する受容体の作用機序の一端を明らかにし、健康や医療に応用される可能性を示すことができた。