Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3

Shannon M. Reilly, Chao Wei Hung, Maryam Ahmadian, Peng Zhao, Omer Keinan, Andrew V. Gomez, Julia H. DeLuca, Benyamin Dadpey, Donald Lu, Jessica Zaid, Bre Anne Poirier, Xiaoling Peng, Ruth T. Yu, Michael Downes, Christopher Liddle, Ronald M. Evans, Anne N. Murphy, Alan R. Saltiel

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)620-634
Number of pages15
JournalNature Metabolism
Volume2
Issue number7
DOIs
StatePublished - Jul 1 2020
Externally publishedYes

ASJC Scopus subject areas

  • Physiology (medical)
  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Cell Biology

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