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

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K00905
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Eating habits
• Research Institution: Seinan 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
• 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

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.

Free Research Field

栄養学

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。