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Cell Rep. 2015 Feb 3;10(4):505-15. doi: 10.1016/j.celrep.2014.12.048. Epub 2015 Jan 22.

Dependence of brown adipose tissue function on CD36-mediated coenzyme Q uptake.

Author information

1
Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA.
2
Department of Electrical Engineering and Computer Sciences, University of California Berkeley, Berkeley, CA 94720, USA.
3
The Buck Institute for Research on Aging, Novato, CA 94945, USA.
4
Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2R3, Canada.
5
Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA. Electronic address: astahl@berkeley.edu.

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.

PMID:
25620701
PMCID:
PMC4318762
DOI:
10.1016/j.celrep.2014.12.048
[Indexed for MEDLINE]
Free PMC Article

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