アディポサイト特有のIGF1Rノックアウトは,男性マウスの食事による肥満と戦うためにβ-カテニン/アペリン軸を活性化します

Haoan Wang1, Ai Mi1, Xiaoshuang Wang1

  • 1Institute of Genome Engineered Animal Models for Human Diseases, National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, China.

PubMed
まとめ

脂肪のインスリン型の成長因子1受容体 (IGF1R) をターゲットにすることで,新しいβ-カタニン/アペリン軸を通じて代謝を再プログラムすることで,肥満と闘います. このアプローチは,高脂肪食のストレスの下で,グルコースのコントロールを改善し,脂肪の蓄積を減少させます.

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