グリコゲン代謝は,グルコースホメオスタシスを脂肪細胞の熱生成と結びつける
Omer Keinan1, Joseph M Valentine1, Haopeng Xiao2,3
1Department of Medicine, University of California San Diego, San Diego, CA, USA.
Nature
|October 28, 2021
まとめ
脂肪細胞におけるグリコゲン代謝は熱生成に不可欠である. カテコラミンは,p38 MAPKを活性化する反応性酸素種を生成し,解離タンパク質1 (UCP1) の発現を促し,エネルギー消費を増加させます.
科学分野:
- 代謝の調節
- 携帯電話のエネルギー支出
- 脂肪細胞の機能
背景:
- 長期の交感活性化により,脂肪細胞における解離タンパク質1 (UCP1) の発現により,エネルギー消費が増加する.
- カテコアミンシグナル伝達と持続したUCP1発現を結びつける正確なメカニズムは,まだ完全に理解されていません.
研究 の 目的:
- UCP1の発現と脂肪細胞の発熱を調節するグリコゲン代謝の役割を調査する.
- カテコロアミン,グリコゲン,UCP1誘導を結びつけるシグナル伝達経路を解明する.
主な方法:
- 脂肪細胞特異的なノックアウトマウスモデルを使用し,グリコゲン (PTG) を標的とするタンパク質が欠けていました.
- 評価されたグリコゲン濃度,UCP1発現,そして寒冷とベータアドレナジック刺激に対する熱生成反応.
- 反応性酸素種生成とp38 MAPKの活性化を分析した.
主要な成果:
- UCP1 を発現する脂肪細胞のグリコゲン蓄積を増加させた.
- 脂肪細胞特異的なPTGの消去はベージュの脂肪細胞グリコゲンを減少させ,UCP1発現を弱め,寒さによる発熱を阻害した.
- カテコラミンの刺激により,反応性酸素種生成とUCP1発現を誘発するp38 MAPKの活性化に必要なグリコゲンの合成と分解が増加した.
結論:
- グライコゲンの代謝は脂肪細胞の発熱に重要な規制的役割を果たします.
- 活性酸素種とp38 MAPKシグナル伝達を通じて,グルコース代謝とUCP1媒介のエネルギー消費を結びつける.
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