食中のフルークトーズは,微生物から派生したアセテットを介して肝臓の脂質生成を供給する
Steven Zhao1,2,3, Cholsoon Jang4, Joyce Liu1,2,5
1Department of Cancer Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Nature
|March 28, 2020
まとめ
フルクトーズは肝臓の脂肪の生成を 2つの経路で促進します 肝臓細胞での直接的な変換と 微生物によるアセテットです 微生物によるアセテット生成を抑制すると,フルークトーゼによる脂肪酸合成が著しく減少する.
科学分野:
- 代謝疾患の研究
- 栄養学
- ヘパトロジー
背景:
- フルクトースの摂取は肥満と脂肪肝に関連しています
- フルクトーザの摂取は,肝臓における新たな脂質生成 (脂肪合成) を促進する.
- フルクトースから肝臓脂肪の蓄積までの正確な経路は不明である.
研究 の 目的:
- 食中の果糖と肝臓のアセチル-CoAと脂質合成を結びつける代謝経路を解明する.
- フルクトースの代謝におけるATPシトラートライアス (ACLY) と腸内微生物の役割を調査する.
主な方法:
- マウスにおける同位体の追跡
- 肝臓特異的な遺伝子消去 (Acly)
- 腸内微生物の減少と 肝臓ACSS2の静止
主要な成果:
- 肝臓特異的なAclyの消去は,フルークトーゼ誘発の脂質生成を防ぐことはできませんでした.
- 腸内微生物群はフルクトースをアセテートに変換し,ACLYとは独立してアセチル-CoAを供給する.
- 微生物群の枯渇またはACSS2の静止は,フルークトーゼを肝臓のアセチル-CoAと脂肪酸に変換することを抑制しました.
- 漸進的なフルークトーズの摂取は肝細胞のシトラート分裂と 微生物アセテットの両方を含んでいた.
- フルクトーズはアセチル-コア代謝とは独立してリポゲン遺伝子発現を活性化させる.
結論:
- 肝臓の脂質生成は,肝細胞の果分分解と微生物のアセテットを含む二重メカニズムによって調節されます.
- 微生物アセテートは,食事によるフルクトースによる脂質性アセチル-コアの主な源である.
- これらの経路を理解することで 代謝疾患の治療に新たな目標が生まれます
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