Anderson Courtney M, Kazantzis Melissa, Wang Jinshan, Venkatraman Subramaniam, Goncalves Renata L S, Quinlan Casey L, Ng Ryan, Jastroch Martin, Benjamin Daniel I, Nie Biao, Herber Candice, Van An-Angela Ngoc, Park Michael J, Yun Dawee, Chan Karen, Yu Angela, Vuong Peter, Febbraio Maria, Nomura Daniel K, Napoli Joseph L, Brand Martin D, Stahl Andreas
Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA.
Department of Electrical Engineering and Computer Sciences, University of California Berkeley, Berkeley, CA 94720, USA.
Cell Rep. 2015 Feb 3;10(4):505-15. doi: 10.1016/j.celrep.2014.12.048. Epub 2015 Jan 22.
Brown adipose tissue (BAT) possesses the inherent ability to dissipate metabolic energy as heat through uncoupled mitochondrial respiration. An essential component of the mitochondrial electron transport chain is coenzyme Q (CoQ). While cells synthesize CoQ mostly endogenously, exogenous supplementation with CoQ has been successful as a therapy for patients with CoQ deficiency. However, which tissues depend on exogenous CoQ uptake as well as the mechanism by which CoQ is taken up by cells and the role of this process in BAT function are not well understood. Here, we report that the scavenger receptor CD36 drives the uptake of CoQ by BAT and is required for normal BAT function. BAT from mice lacking CD36 displays CoQ deficiency, impaired CoQ uptake, hypertrophy, altered lipid metabolism, mitochondrial dysfunction, and defective nonshivering thermogenesis. Together, these data reveal an important new role for the systemic transport of CoQ to BAT and its function in thermogenesis.
棕色脂肪组织（BAT）具有通过解偶联线粒体呼吸将代谢能量以热量形式消散的内在能力。线粒体电子传递链的一个重要组成部分是辅酶Q（CoQ）。虽然细胞大多通过内源性方式合成CoQ，但外源性补充CoQ已成功用于治疗CoQ缺乏症患者。然而，哪些组织依赖外源性CoQ摄取以及CoQ被细胞摄取的机制及其在BAT功能中的作用尚不清楚。在此，我们报告清道夫受体CD36驱动BAT对CoQ的摄取，并且是正常BAT功能所必需的。缺乏CD36的小鼠的BAT表现出CoQ缺乏、CoQ摄取受损、肥大、脂质代谢改变、线粒体功能障碍以及非寒战产热缺陷。总之，这些数据揭示了CoQ向BAT的全身转运及其在产热中的功能的一个重要新作用。
