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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.
Abstract

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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