Journal
CELL METABOLISM
Volume 26, Issue 5, Pages 753-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2017.09.004
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Funding
- Fondation Leducq Transatlantic Network [12CVD04]
- Louis-Jeantet Prize for Medicine
- European Research Council (ERC) under the European Union's Seventh Framework Programme/ERC [340896]
- LipoCheX
- Austrian Science Fund (FWF) [Z136, SFB LIPOTOX F3001/F3002]
- NIH [R03-DK-077697, R01-DK-090166]
- NAWI Graz
- [P28882-B21]
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Fatty acids (FAs) activate and fuel UCP1-mediated non-shivering thermogenesis (NST) in brown adipose tissue (BAT). Release of FAs from intracellular fat stores by adipose triglyceride lipase (ATGL) is considered a key step in NST. Accordingly, the severe cold intolerance of global ATGL knockout (AKO) mice has been attributed to defective BAT lipolysis. Here we show that this conclusion is incorrect. We demonstrate that although the BAT-specific loss of ATGL impairs BAT lipolysis and alters BAT morphology, it does not compromise the beta(3)-adrenergic thermogenic response or cold-induced NST. Instead, NST depends on nutrient supply or lipolysis in white adipose tissue during fasting, suggesting that circulating energy substrates are sufficient to fuel NST. Cold intolerance in AKO mice is not caused by BAT dysfunction as previously suspected but by severe cardiomyopathy. We conclude that functional NST requires adequate substrate supply and cardiac function, but does not depend on ATGL-mediated lipolysis in BAT.
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