CRTC3は,カテキオラミンシグナリングをエネルギーバランスと結びつけています
Youngsup Song1, Judith Altarejos, Mark O Goodarzi
1The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.
Nature
|December 18, 2010
まとめ
コアクティベーターCrtc3は,脂肪細胞内のβ-アドレナリン受容体の効果を弱めることによって,肥満を促進する. CRTC3の一般的な変種は,ヒトの集団における肥満と関連しています.
科学分野:
- メタボリック調節 メタボリック調節
- アディポス組織生物学
- 肥満に関する研究.
背景:
- レプチンは,交感神経系の活性化を介してエネルギーバランスを調節します.
- アディポサイトにおけるベータアドレネルジック受容体のシグナル伝達は,脂解と脂肪酸の酸化を通じたエネルギー消費を誘導する.
- カテコロアミンのシグナル伝達の障害は,肥満とインスリン抵抗性に関連しています.
研究 の 目的:
- 肥満におけるCREB共活性化剤Crtc3の役割を調査する.
- Crtc3が脂肪組織におけるβ-アドレナergic受容体シグナル伝達に影響を与えるメカニズムを解明する.
主な方法:
- カテコアミン信号への反応としてCrtc3の活性化が研究された.
- アデニルサイクラース活性とRgs2発現に対するCrtc3の影響を評価した.
- ヒトのCRTC3変異と,メキシコ系アメリカ人のコホートにおける肥満の関連性を調べました.
主要な成果:
- Crtc3は,脂肪組織におけるβ-アドレナergic受容体シグナル伝達を弱めることが判明しました.
- Crtc3の活性化により,Rgs2の発現を向上させることで,アデニルサイクラースの活性が低下した.
- 肥満と相関するより高い転写活性を持つ一般的なヒトCRTC3変異体.
結論:
- アディポサイトCrtc3は,肥満を促進する役割を果たします.
- Crtc3は,脂肪細胞のシグナル伝達に及ぼす影響により,ヒトにおける肥満の発生に寄与する可能性がある.
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