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Research for preventive nutrition and molecular basis of mitochondrial disfunction and of compensatory folate hypermetabolic

Research Project

Project/Area Number 17K00905
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Eating habits
Research InstitutionSeinan Jo Gakuin University

Principal Investigator

Amamoto Rie  西南女学院大学, 保健福祉学部, 准教授 (00352344)

Co-Investigator(Kenkyū-buntansha) 内海 健  九州大学, 医学研究院, 教授 (80253798)
Project Period (FY) 2017-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywordsミトコンドリア機能異常 / 葉酸代謝 / 一炭素代謝 / 心筋細胞 / 心臓組織 / p32タンパク質 / ミトコンドリア / 心疾患
Outline of Final Research Achievements

The relationship between folate metabolism and lifestyle-related diseases such as arteriosclerosis, cancer, and dementia has attracted attention, and it has been reported that insufficient intake of folic acid is a risk factor for these diseases. In this study, we speculated that the enhancement of mitochondrial folic acid and amino acid metabolism functions as a compensatory defense mechanism against the deterioration of the pathological condition due to mitochondrial function decline. Given that mitochondrial dysfunction is one of the causes of aging and lifestyle-related diseases, it is expected that the intake of folic acid will play a role in their prevention and prevention of aggravation.

Academic Significance and Societal Importance of the Research Achievements

ミトコンドリア内での葉酸代謝の亢進は、癌や胎児の細胞では見られるが、正常細胞ではあまり見られない。中でもミトコンドリアの葉酸代謝酵素であるMthfd2は、正常の細胞での発現はないと言われている。本研究で用いたミトコンドリア機能異常の心筋細胞では、この酵素の発現が見られ、葉酸、アミノ酸代謝を亢進させ、ミトコンドリアにおけるエネルギー代謝機能の低下を補っていることが考えられた。生活習慣病予防のためにも積極的な葉酸摂取を推奨するための基礎となる結果が得られたと考える。

Report

(4 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report
  • Research Products

    (3 results)

All 2019 2017

All Journal Article (2 results) (of which Peer Reviewed: 2 results,  Open Access: 2 results) Presentation (1 results)

  • [Journal Article] Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses2017

    • Author(s)
      Saito Toshiro、Uchiumi Takeshi、Yagi Mikako、Amamoto Rie、Setoyama Daiki、Matsushima Yuichi、Kang Dongchon
    • Journal Title

      Cardiovascular Research

      Volume: 113 Issue: 10 Pages: 1173-1185

    • DOI

      10.1093/cvr/cvx095

    • Related Report
      2017 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration2017

    • Author(s)
      Yagi Mikako、Uchiumi Takeshi、Sagata Noriaki、Setoyama Daiki、Amamoto Rie、Matsushima Yuichi、Kang Dongchon
    • Journal Title

      Scientific Reports

      Volume: 7 Issue: 1

    • DOI

      10.1038/s41598-017-15414-5

    • Related Report
      2017 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] ミトコンドリア機能異常と葉酸代謝亢進との関連性の検討2019

    • Author(s)
      天本理恵、八木美佳子、内海健
    • Organizer
      第66回日本栄養改善学会
    • Related Report
      2019 Annual Research Report

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Published: 2017-04-28   Modified: 2021-02-19  

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