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代謝 適応 は 血熱 症 に 対する 耐性 を 確立 する
Sebastian Weis1, Ana Rita Carlos2, Maria Raquel Moita2
1Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal; Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, 07747 Jena, Germany.
Cell
|June 17, 2017
まとめ
セプシスに対する耐性は,鉄とグルコースの代謝を調節するフェリチンH鎖 (FTH) に依存する. このメカニズムは低血糖症を予防し,感染中に宿主ホメオスタシスを維持します.
科学分野:
- 免疫学
- メタボリックシンドローム
- 病理生理学
背景:
- セプシスは生命を脅かす病気で 免疫機能と代謝反応が 調節不能に なることによるものです
- 病原菌を直接傷つけることなく ホメオスタシスを維持する宿主の防御戦略です
研究 の 目的:
- セプシスに対する耐性の確立におけるフェリチンH鎖 (FTH) の役割を調査する.
- FTHがセプシス誘発の低血糖症に対する保護を与えるメカニズムを解明する.
主な方法:
- 多微生物感染に対するFTH誘導
- 肝臓のグルコース6ファスファターゼ (G6Pase) 活性に対するFTHの効果の評価
- 固有のグルコース生成とグルコネ生成の評価
- FTHまたはフェリチンの治療用投与
主要な成果:
- FTH誘導はセプシスの耐性には極めて重要です.
- FTHは,G6Paseの鉄による酸化阻害から保護します.
- 持続的なグルコネオゲネシスは低血糖症を予防し,疾患耐性を保ちます.
- FTHの過剰発現やフェリチン投与が治療効果を示した.
結論:
- セプシス症の耐性は,鉄とグルコースの代謝の間の重要な相互作用を伴う.
- FTHによる鉄とグルコースの調節は,血糖の恒常性を維持するために不可欠です.
- 鉄とグルコースの代謝を標的とした治療は セプシスの治療策です
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