| First Author | Reilly SM | Year | 2020 |
| Journal | Nat Metab | Volume | 2 |
| Issue | 7 | Pages | 620-634 |
| PubMed ID | 32694788 | Mgi Jnum | J:309241 |
| Mgi Id | MGI:6757598 | Doi | 10.1038/s42255-020-0217-6 |
| Citation | Reilly SM, et al. (2020) Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3. Nat Metab 2(7):620-634 |
| abstractText | 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 beta-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. |
