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Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3.
- Author(s): Reilly, Shannon M
- Hung, Chao-Wei
- Ahmadian, Maryam
- Zhao, Peng
- Keinan, Omer
- Gomez, Andrew V
- DeLuca, Julia H
- Dadpey, Benyamin
- Lu, Donald
- Zaid, Jessica
- Poirier, BreAnne
- Peng, Xiaoling
- Yu, Ruth T
- Downes, Michael
- Liddle, Christopher
- Evans, Ronald M
- Murphy, Anne N
- Saltiel, Alan R
- et al.
Published Web Location
https://doi.org/10.1038/s42255-020-0217-6Abstract
Catecholamines stimulate the mobilization of stored triglycerides in adipocytes to provide fatty acids (FAs) for other tissues. However, a large proportion is taken back up and either oxidized or re-esterified. What controls the disposition of these FAs in adipocytes remains unknown. Here, we report that catecholamines redirect FAs for oxidation through the phosphorylation of signal transducer and activator of transcription 3 (STAT3). Adipocyte STAT3 is phosphorylated upon activation of β-adrenergic receptors, and in turn suppresses FA re-esterification to promote FA oxidation. Adipocyte-specific Stat3 KO mice exhibit normal rates of lipolysis, but exhibit defective lipolysis-driven oxidative metabolism, resulting in reduced energy expenditure and increased adiposity when they are on a high-fat diet. This previously unappreciated, non-genomic role of STAT3 explains how sympathetic activation can increase both lipolysis and FA oxidation in adipocytes, revealing a new regulatory axis in metabolism.
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