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腸から脳へのシグナリングは,食中のタンパク質の摂取を制限します

Nikolai P Jaschke¹, Joseph R Luchsinger², Zuojia Chen³

¹Department of Immunobiology, Yale School of Medicine, New Haven, CT 06510, USA; Department of Internal Medicine (Rheumatology, Allergy, and Immunology), Yale School of Medicine, New Haven, CT 06510, USA; Department of Medicine I & III, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Hamburg Center for Translational Immunology, Hamburg, Germany.

|November 5, 2025

まとめ

回復しているマウスは驚くべきことにタンパク質の摂取を制限しグルタミンリスントレオニンなどの特定のアミノ酸を避けます腸のアンモニア感知によって適応する行動は病気の回復過程で毒性を防ぐのに役立ちます

科学分野:

栄養神経科学
胃腸内科
生理学

背景:

栄養素の最適な摂取量は生理的状態によって異なりますが,食事のセットポイントを調整するメカニズムは不明です.
回復の生理学を理解することは病理的回復の病気に対処するために不可欠です

研究の目的:

カタボリック状態からの回復過程における適応的な食物好みの生理学的基礎を調査する.
回復時に嫌悪を誘発する特定の栄養素を特定し,その背後にあるメカニズムを明らかにする.

主な方法:

カタボリック状態からの回復中にマウスの食事摂取パターンを観察した.
タンパク質嫌悪の原因となる重要なアミノ酸 (グルタミン,ライシン,スレオニン) を特定した.
腸内アンモニアゲネシス,エンテロクロマフィン細胞,TRPA1チャンネル,セロトニンシグナル伝達が食欲不振を媒介する役割を調査した.

主要な成果:

意識的にタンパク質の摂取を制限し回復期間中のカロリー摂取を優先しました
グルタミン,ライシン,スレオニンはタンパク質嫌悪を誘発するのに必要で十分であると特定されました.
嫌悪反応には,腸内アンモニア生成,TRPA1に依存したエンテロクロマフィン細胞による感知,および脳幹へのセロトニン信号が含まれます.

結論:

新しい"回復行動"のメカニズムが特定され,適応的な食事の好みによって特徴づけられました.
この行動は特定のアミノ酸とアンモニアの生成によって引き起こされる腸-脳信号経路によって媒介されます
発見は,回復障害に関連した病気を理解し,治療し,回復を促進する介入の開発に意味を持っています.

キーワード:

TRPA1 についてアミノ酸アンモニア食事中のタンパク質腸-脳軸高タンパク質の食事プロテイン・レバレッジ回復する尿素サイクル

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