レプチン調節されたエンドカンナビノイドは,食物摂取の維持に関与しています
V Di Marzo1, S K Goparaju, L Wang
1Endocannabinoid Research Group, Istituto per la Chimica di Molecole di Interesse Biologico, CNR, 80072, Arco Felice, Naples, Italy.
Nature
|April 12, 2001
まとめ
視床下部のエンドカンナビノイドはCB1受容体を活性化し,食物摂取に影響を与えます. レプチンのシグナル伝達欠陥は,エンドカンナビノイドを増加させ,肥満とエネルギーバランスの役割を示唆します.
科学分野:
- 神経科学は神経科学である.
- エンドクリノロジー エンドクリノロジー
- メタボリズムは
背景:
- レプチンは,食欲とエネルギーバランスを下垂体シグナル伝達を通じて調節する重要なホルモンです.
- 肥満は,レプチンまたはメラノコルチンの経路の遺伝的欠陥に起因する可能性があります.
- CB1受容体を含むような食欲を刺激する別の経路が存在する.
研究 の 目的:
- 下垂体におけるCB1カンナビノイド受容体とエンドカンナビノイドの役割を調査する.
- レプチンシグナル伝達とエンドカンナビノイドレベルとの関係を決定する.
- レプチンと食欲の調節を結びつける神経回路を探求する.
主な方法:
- CB1受容体ノックアウトマウスと野生型の littermates を利用しました.
- 投与されたCB1アンタゴニストSR141716A.
- 様々な肥満マウスモデル (db/db, ob/ob) とラットで,下体内内カンナビノイドレベルを測定した.
- エンドカンナビノイドレベルに対する急性レプチン治療の効果を評価した.
主要な成果:
- CB1受容体ノックアウトマウスは,対照群と比較して,食物制限後に摂取量の減少を示した.
- SR141716A 野生型のマウスの食物摂取量が減ったが,ノックアウトマウスの場合はそうではない.
- レプチン欠乏症の肥満モデルでは,下垂体内カンナビノイドの値が上昇した.
- レプチン治療は,正常および肥満マウスの下体内内カンナビノイドレベルを低下させた.
結論:
- CB1受容体に作用する下体内カンナビノイドは,食物摂取をトニック的に刺激する可能性があります.
- エンドカンナビノイドシグナル伝達は,レプチンによって調節される神経経路に関与しています.
- この経路は,食欲とエネルギーバランスの管理のための潜在的なターゲットです.
関連する概念動画
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