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线粒体ROS调节UCP1的热能消耗和硫化

Edward T Chouchani^1,2, Lawrence Kazak^1,2, Mark P Jedrychowski²

¹Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

|March 31, 2016

概括

线粒体反应性氧物种 (ROS) 对于棕色脂肪组织热生成至关重要. 这一发现为肥胖和糖尿病等代谢障碍提供了新的治疗点.

科学领域:

细胞生物学
代谢研究
脂肪组织生物学

背景情况:

棕色和色脂肪组织通过热性呼吸,依赖于解蛋白1 (UCP1) 来消散能量.
脂肪细胞中的UCP1依赖热生成具有对抗肥胖和糖尿病的潜力.
了解控制UCP1依赖呼吸的因素对于代谢疾病治疗至关重要.

研究的目的:

研究线粒体反应性氧物种 (ROS) 在棕色脂肪组织 (BAT) 热生成中的作用.
确定ROS是否对UCP1依赖的呼吸和全身能量消耗至关重要.
阐明ROS调节UCP1活动的分子机制.

主要方法:

激发棕色脂肪组织中的热生成.
对线粒体ROS水平的药理操作.
测量UCP1依赖的呼吸和全身能量消耗.
分析囊醇氧化还原状态和蛋白质硫化,特别是针对UCP1 Cys253.

主要成果:

在BAT中,急性激活热生成的特征是线粒体ROS水平的增加.
线粒体ROS的药理性耗尽损害了体内热生成,并减少了UCP1依赖的能量消耗.
热生成的ROS改变了BAT中的囊二醇的氧化还原状态,增强了呼吸.
在热生成过程中,UCP1Cys253被硫化,其突变会影响UCP1活性和上腺激活.

结论:

在棕色脂肪组织中的线粒体ROS诱导是支持UCP1依赖热生成的关键机制.
通过ROS调节UCP1对于全身能量消耗至关重要.
这些发现为治疗肥胖和糖尿病等代谢障碍找到了新的途径.

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