在棕色脂肪线粒体中依赖脂肪酸的UCP1脱的机制
Andriy Fedorenko1, Polina V Lishko, Yuriy Kirichok
1Department of Physiology, University of California San Francisco, UCSF Mail Code 2140, Genentech Hall Room N272F, 600 16th Street, San Francisco, CA 94158, USA.
Cell
|October 16, 2012
概括
线粒体解蛋白1 (UCP1) 作为脂肪酸阳离子/质子同载体. 这种机制使棕色脂肪线粒体能够产生热量而不是ATP,调节代谢效率.
科学领域:
- 线粒体生理学线粒体生理学
- 生物化学 生物化学
- 细胞代谢的细胞代谢.
背景情况:
- 线粒体解蛋白1 (UCP1) 在棕色脂肪组织 (BAT) 中驱动非的热生成.
- 通过长链脂肪酸 (LCFA) 激活UCP1,增加了内部线粒体膜 (IMM) 电导率,将热量产生与ATP合成脱.
- 通过UCP1介导的质子运输的精确机制仍然未解决.
研究的目的:
- 为了阐明UCP1.1的传输机制.
- 为了确定LCFA如何激活UCP1进行热生成.
主要方法:
- 在BAT线粒体内线粒体膜上进行了UCP1电流的直接补丁测量.
- 对UCP1与LCFA和质子运输的相互作用进行分析.
主要成果:
- UCP1作为一个长链脂肪酸离子/H(+) 配送体.
- 由于疏水性相互作用,LCFA离子仍然与UCP1结合,使UCP1能够充当H ((+) 载体.
- 这种依赖LCFA的机制促进了跨膜质子运输.
结论:
- UCP1作为LCFA激活的质子载体运行,对于非热生成至关重要.
- 这些发现解决了长期以来关于UCP1的传输机制的问题.
- 类似的机制可以通过SLC25家族成员调节其他组织的代谢效率.
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