Fto遺伝子の非活性化により,肥満から保護されます
Julia Fischer1, Linda Koch, Christian Emmerling
1Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitätsstr. 1, D-40225 Düsseldorf, Germany.
Nature
|February 24, 2009
まとめ
FTO遺伝子は肥満のリスクと関連しています. マウスのFtoの減少は,体脂肪と筋量減少を引き起こし,エネルギー消費と体重の調節におけるその役割を明らかにしました.
科学分野:
- 遺伝学 遺伝学とは
- メタボリズムは
- 肥満に関する研究
背景:
- ゲノム全体の関連研究は,ヒトのFTO遺伝子ポリモルフィズムとボディマス指数と肥満リスクとを関連付けています.
- FTOの第1イントロンの一般的な変異は,体重増加と関連しており,特にリスクアレルのホモジゴーツではそうである.
- エネルギーホメオスタシスを調節するFTOの正確な機能は,ほとんど不明のままです.
研究 の 目的:
- エネルギーホメオスタシスと体質調節におけるFTO遺伝子の機能的役割を調査する.
- 哺乳類モデルのFto機能喪失の生理学的結果を決定する.
主な方法:
- Fto欠乏症のマウスを生成し,遺伝子喪失の影響を研究した.
- 評価された体組成,脂肪組織と痩身量を含む.
- 測定されたエネルギー消費と監視された活動レベルと食物の摂取量.
主要な成果:
- Fto欠乏したマウスは,産後成長遅延を示した.
- Fto欠乏マウスでは,脂肪組織と体量の両方の有意な減少が観察されました.
- これらのマウスの痩身は,活動が低下し,食物摂取が増加したにもかかわらず,エネルギー消費の増加と交感神経系の活性化に起因する.
結論:
- この研究は,Ftoがエネルギーホメオスタシスに決定的な役割を果たすという最初の直接的な証拠を提供します.
- Ftoはエネルギー消費を調節し,体質と組成に影響を与えます.
- これらの発見は,肥満と代謝障害の潜在的な治療目標としてFTOを強調しています.
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