Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3
| Autor: | Jessica Zaid, Christopher Liddle, Alan R. Saltiel, Xiaoling Peng, Omer Keinan, Maryam Ahmadian, BreAnne Poirier, Julia H DeLuca, Peng Zhao, Chao-Wei Hung, Benyamin Dadpey, Donald Lu, Michael Downes, Shannon M. Reilly, Ruth T. Yu, Andrew V. Gomez, Ronald M. Evans, Anne N. Murphy |
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| Rok vydání: | 2019 |
| Předmět: |
STAT3 Transcription Factor
medicine.medical_specialty Endocrinology Diabetes and Metabolism Lipolysis Adipocytes White Fatty Acids Nonesterified Diet High-Fat Article chemistry.chemical_compound Mice Catecholamines Physiology (medical) Adipocyte Internal medicine Internal Medicine medicine Animals Obesity Phosphorylation STAT3 Receptor chemistry.chemical_classification Mice Knockout biology Fatty acid Esters Cell Biology Metabolism Adrenergic beta-Agonists Mice Inbred C57BL Endocrinology chemistry STAT protein biology.protein Energy Metabolism Oxidation-Reduction |
| Zdroj: | Nature metabolism |
| ISSN: | 2522-5812 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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