カルシントニン3β-S100b軸経由で発熱性脂肪組織の神経化
Xing Zeng1,2, Mengchen Ye3, Jon M Resch4
1Department of Cancer Biology, Dana Farber Cancer Institute, Boston, MA, USA.
Nature
|May 3, 2019
まとめ
発熱性アディポサイトは,カルシンテニン3βという新しいタンパク質を介して,交感性ニューロンと通信する. この相互作用は脂肪の発熱を調節し,マウスの食事による肥満から保護します.
科学分野:
- メタボリズム
- 神経内分泌学
- 細胞生物学
背景:
- 交感神経系は,ノラドレナリン経由で,茶色とベージュの脂肪細胞の発熱を調節する.
- 発熱性脂肪のシンパティック・インナーベーションの増加の背後にある分子メカニズムは不明である.
研究 の 目的:
- 発熱性アディポサイトの交感性インナーベーションの強化の分子基盤を調査する.
- 脂肪細胞と交感神経細胞の間のコミュニケーションに関与する新しい要因を特定する.
主な方法:
- 脂肪細胞におけるカルシントニン3βの遺伝子操作 (機能の喪失と獲得) を利用した.
- 脂肪組織における交感内膜の評価
- カルシントニン3βがS100bの分泌に与える効果と,同情神経細胞に与える影響をインビトロで分析した.
- カルシントニン3β欠乏がマウスの食事による肥満に与える影響を研究した.
主要な成果:
- 発熱性脂肪細胞で哺乳類特異的なエンドプラズマ網膜タンパク質であるカルシントニン3βを特定した.
- カルシントニン3βの遺伝的調節により,脂肪組織における交感内置が変化した.
- カルシントニン3βはS100bの分泌を促進し,交感神経細胞の増殖を刺激する.
- カルシントニン3βの消去は,高脂肪食のマウスの肥満を引き起こし,S100bの欠乏をフェノコピングした.
結論:
- 発熱性アディポサイトと交感性ニューロン間のコミュニケーションを介する哺乳類特有の新しいメカニズムを発見した.
- カルシントニン3β-S100b経路は,交感内置の調節と肥満の予防に不可欠です.
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