Elucidation of the molecular mechanism of the effect of androgens on the maintenance and the hypertrophy of skeletal muscle mass.

2022 Fiscal Year Final Research Report

• Project/Area Number: 21K17568
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 59020:Sports sciences-related
• Research Institution: Ehime University
• Principal Investigator: Sakai Hiroshi 愛媛大学, プロテオサイエンスセンター, 助教 (00820804)
• Project Period (FY): 2021-04-01 – 2023-03-31
• Keywords: アンドロゲン / 男性ホルモン / アンドロゲン受容体 / 骨格筋 / 間葉系前駆細胞

Outline of Final Research Achievements

The purpose of this study was to generate mesenchymal progenitor cell-specific, androgen receptor-deficient mice and to analyze their phenotype. First, we generated mesenchymal progenitor cell-specific AR-deficient mice (PDGFRα-CreER;ARf/y). However, no differences were observed in skeletal muscle at steady state, both in weight and number and size of myofibers. In addition, a high-fat diet was administered to induce adipocytes in the skeletal muscle tissue. However, no differences were observed in body weight, muscle weight, visceral and subcutaneous fat mass, or fat mass within skeletal muscle. These results suggest that androgen receptor function in mesenchymal progenitor cells is limited to skeletal muscle in the steady state and in the adipose-induced state.

Free Research Field

スポーツ科学

Academic Significance and Societal Importance of the Research Achievements

本研究では、間葉系前駆細胞特異的に、アンドロゲン受容体を欠損させたマウスを作出し、その表現型を解析することで、アンドロゲンと間葉系前駆細胞の関係を詳細に解明した。この作用機序を解明することは、アンドロゲン補充治療の副作用を解明し、サルコペニアの予防・治療の発展と、ひいては超高齢社会における健康寿命問題を克服する一つの起点となる。