| Literature DB >> 25620701 |
Courtney M Anderson1, Melissa Kazantzis1, Jinshan Wang1, Subramaniam Venkatraman2, Renata L S Goncalves3, Casey L Quinlan3, Ryan Ng3, Martin Jastroch3, Daniel I Benjamin1, Biao Nie1, Candice Herber1, An-Angela Ngoc Van1, Michael J Park1, Dawee Yun1, Karen Chan1, Angela Yu1, Peter Vuong1, Maria Febbraio4, Daniel K Nomura1, Joseph L Napoli1, Martin D Brand3, Andreas Stahl5.
Abstract
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.Entities:
Mesh：
Substances：
Year: 2015 PMID： 25620701 PMCID： PMC4318762 DOI： 10.1016/j.celrep.2014.12.048
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423