Dependence of Brown Adipose Tissue Function on CD36-Mediated Coenzyme Q Uptake

Courtney M. Anderson; Melissa Kazantzis; Jinshan Wang; Subramaniam Venkatraman; Renata L.S. Goncalves; Casey L. Quinlan; Ryan Ng; Martin Jastroch; Daniel I. Benjamin; Biao Nie; Candice Herber; An-Angela Ngoc Van; Michael J. Park; Dawee Yun; Karen Chan; Angela Yu; Peter Vuong; Maria Febbraio; Daniel K. Nomura; Joseph L. Napoli; Martin D. Brand; Andreas Stahl

doi:10.1016/j.celrep.2014.12.048

Cell Reports (Feb 2015)

Dependence of Brown Adipose Tissue Function on CD36-Mediated Coenzyme Q Uptake

Courtney M. Anderson,
Melissa Kazantzis,
Jinshan Wang,
Subramaniam Venkatraman,
Renata L.S. Goncalves,
Casey L. Quinlan,
Ryan Ng,
Martin Jastroch,
Daniel I. Benjamin,
Biao Nie,
Candice Herber,
An-Angela Ngoc Van,
Michael J. Park,
Dawee Yun,
Karen Chan,
Angela Yu,
Peter Vuong,
Maria Febbraio,
Daniel K. Nomura,
Joseph L. Napoli,
Martin D. Brand,
Andreas Stahl

Affiliations

Courtney M. Anderson: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Melissa Kazantzis: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Jinshan Wang: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Subramaniam Venkatraman: Department of Electrical Engineering and Computer Sciences, University of California Berkeley, Berkeley, CA 94720, USA
Renata L.S. Goncalves: The Buck Institute for Research on Aging, Novato, CA 94945, USA
Casey L. Quinlan: The Buck Institute for Research on Aging, Novato, CA 94945, USA
Ryan Ng: The Buck Institute for Research on Aging, Novato, CA 94945, USA
Martin Jastroch: The Buck Institute for Research on Aging, Novato, CA 94945, USA
Daniel I. Benjamin: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Biao Nie: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Candice Herber: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
An-Angela Ngoc Van: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Michael J. Park: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Dawee Yun: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Karen Chan: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Angela Yu: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Peter Vuong: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Maria Febbraio: Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2R3, Canada
Daniel K. Nomura: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Joseph L. Napoli: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA
Martin D. Brand: The Buck Institute for Research on Aging, Novato, CA 94945, USA
Andreas Stahl: Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, USA

DOI: https://doi.org/10.1016/j.celrep.2014.12.048
Journal volume & issue: Vol. 10, no. 4
pp. 505 – 515

Abstract

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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.

Published in Cell Reports

ISSN: 2211-1247 (Online)
Publisher: Elsevier
Country of publisher: Netherlands
LCC subjects: Science: Biology (General)
Website: http://www.cell.com/cell-reports/home

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