Journal
CELL METABOLISM
Volume 27, Issue 1, Pages 195-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2017.10.008
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Funding
- NIH [R01DK094004, R01CA196986]
- Leukemia and Lymphoma Society Career Development Award
- American Heart Association [15POST25550079]
- American Diabetes Association [1-16-PMF-008]
- Novo Nordisk Foundation
- TrygFonden
- Danish National Research Foundation [DNRF55]
- Danish Council for Strategic Research [09-067009, 09-075724]
- NNF Center for Basic Metabolic Research [Schéele Group] Funding Source: researchfish
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Brown adipose tissue (BAT) is a therapeutic target for metabolic diseases; thus, understanding its metabolic circuitry is clinically important. Many studies of BAT compare rodents mildly cold to those severely cold. Here, we compared BAT remodeling between thermoneutral and mild-cold-adapted mice, conditions more relevant to humans. Although BAT is renowned for catabolic beta-oxidative capacity, we find paradoxically that the anabolic de novo lipogenesis (DNL) genes encoding ACLY, ACSS2, ACC, and FASN were among the most upregulated by mild cold and that, in humans, DNL correlates with Ucp1 expression. The regulation and function of adipocyte DNL and its association with thermogenesis are not understood. We provide evidence suggesting that AKT2 drives DNL in adipocytes by stimulating ChREBP beta transcriptional activity and that cold induces the AKT2-ChREBP pathway in BAT to optimize fuel storage and thermogenesis. These data provide insight into adipocyte DNL regulation and function and illustrate the metabolic flexibility of thermogenesis.
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