ニコチンは,POMCニューロンの活性化により,食物の摂取量を減少させます
Yann S Mineur1, Alfonso Abizaid, Yan Rao
1Department of Psychiatry, Yale University School of Medicine, 34 Park Street, Third Floor Research, New Haven, CT 06508, USA.
Science (New York, N.Y.)
|June 11, 2011
まとめ
喫煙によるニコチンは,食物摂取を制御する特定の脳受容体を活性化することによって食欲を減少させます. この研究は,喫煙が体重にどのように影響するかを明らかにし,肥満と禁煙治療のターゲットを提供します.
科学分野:
- 神経生物学 神経生物学とは
- エンドクリノロジー エンドクリノロジー
- 薬理学 薬理学とは
背景:
- 喫煙は食欲の減少と体重管理と関連しています.
- 禁煙と肥満の治療法を開発するために,喫煙の食欲低下効果の神経生物学的な基礎を理解することは極めて重要です.
研究 の 目的:
- ニコチン誘発の食欲抑制の背後にある神経生物学的メカニズムを解明する.
- 食物摂取と体重に対するニコチンの影響に関与する特定の神経経路と受容体を特定する.
主な方法:
- 薬理学,分子遺伝学,電気生理学,およびマウスの飼育の研究の組み合わせを使用しました.
- ヒポタラム内ニコチンアセチルコリン受容体とメラノコルチン系の役割を研究した.
主要な成果:
- ヒポタラム α3β4 ニコチンアセチルコリン受容体の活性化は,プロオピオメラノコルチン (POMC) ニューロンを刺激する.
- POMCニューロンとメラノコルチン4受容体は,ニコチンの食欲抑制効果をマウスに与えるために不可欠です.
- ニコチンは,体内のメラノコルチン系を介して,食物の摂取量と体重を減らすことが示されました.
結論:
- ニコチンは,下垂体メラノコルチン系を調節することによって,食物の摂取量と体重を減少させます.
- ニコチンの食欲抑制効果の基礎となる主要な分子およびシナプスメカニズムを特定した.
- 禁煙と肥満管理のための新しい治療戦略のための基盤を提供します.
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