A novel nutritional approach to muscle atrophy: Connecting iron and energy metabolism

2019 Fiscal Year Final Research Report

• Project/Area Number: 18K17968
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 59040:Nutrition science and health science-related
• Research Institution: The University of Tokushima
• Principal Investigator: UCHIDA Takayuki 徳島大学, 大学院医歯薬学研究部(医学域), 助教 (00803561)
• Project Period (FY): 2018-04-01 – 2020-03-31
• Keywords: アコニターゼ / ミトコンドリア / 筋萎縮

Outline of Final Research Achievements

In this study, I examined mitochondrial aconitase, a rate-limiting enzyme of TCA cycle, in the progression of muscle atrophy. During the research period from FY2018 to FY2018, I revealed a decrease in slow muscle type myosin heavy chain protein by knockdown of aconitase in C2C12 muscle cells. Furthermore, studies using various inhibitors suggested that matrix metalloprotease is involved in the degradation of myosin protein by aconitase knockdown. Moreover, aconitase deletion induced a decrease in intracellular ATP level, impairment aerobic metabolism by mitochondria, and enhancement of anaerobic metabolism.

Free Research Field

栄養学および健康科学関連

Academic Significance and Societal Importance of the Research Achievements

本研究はTCAサイクル上の重要な酵素であるアコニターゼの筋萎縮における役割について検証した、初めての研究成果である。さらに、エネルギー代謝と筋萎縮の関連性について新たな見地を切り開く点において学術的意義がある。これらの研究成果は、エネルギー代謝が筋量維持に重要であることを示し、ミトコンドリアを介したエネルギー代謝の賦活化が筋萎縮予防につながる可能性を示した点において社会的意義がある。