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2021 Fiscal Year Final Research Report

Clarification of the regulatory mechanism of ACC2, a regulator of beta-oxidation, by biotin and its application to the prevention of the metabolic syndrome

Research Project

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Project/Area Number 18K17974
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 59040:Nutrition science and health science-related
Research InstitutionKobe University (2021)
University of Nagasaki (2018-2020)

Principal Investigator

Yuasa Masahiro  神戸大学, 人間発達環境学研究科, 助教 (00756174)

Project Period (FY) 2018-04-01 – 2022-03-31
Keywordsビオチン / アセチルCoAカルボキシラーゼ(ACC)2 / カルニチンパルミトイルトランスフェラーゼ / β酸化 / エネルギー消費量 / 脂肪消費量 / 肝臓 / 褐色脂肪組織
Outline of Final Research Achievements

In this study, we investigated the mechanism of biotin-induced inhibition of β-oxidation regulator acetyl CoA carboxylase 2 (ACC2) to prevent and improve metabolic syndrome (MS).
Short-term oral administration of high-dose biotin reduced ACC2 gene expression in the rat liver, but long-term oral administration of safe-dose biotin did not change the hepatic ACC2 gene expression. In both of these experiments, an increase in fat oxidation and plasma adiponectin, and a decrease in white adipose tissue were induced; therefore, biotin may be effective in preventing and improving MS; but the liver ACC2 is not the only factor involved in this mechanism.

Free Research Field

基礎栄養学

Academic Significance and Societal Importance of the Research Achievements

将来的には,MSや生活習慣病の予防のためのビオチンによる栄養療法の提案に資すると考える.現在,食品成分によるMSの予防・改善効果に関する検討が多数行われているが,高濃度での継続的な摂取が肝機能障害を生じさせるなどの副作用がある成分も存在する.一方,本研究で採用したビオチン濃度はヒトにおける過剰症が生じない濃度であり,動物実験レベルでは肝機能マーカーを変動させないことが確認されている.このような安全性を踏まえると,ヒトの健康維持・増進に対しても展開可能な栄養療法として,ビオチンが利用できると考える.

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Published: 2023-01-30  

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