Journal
OBESITY
Volume 25, Issue 1, Pages 85-93Publisher
WILEY
DOI: 10.1002/oby.21679
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Funding
- Miguel Servet Fund from Carlos III National Institute of Health, Spain
- Ministerio de Ciencia e Innovacion [SAF2014-55725]
- Instituto de Salud Carlos III
- Fondo Europeo de Desarrollo Regional (FEDER), Madrid, Spain [CP15/00106]
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Objective: Since oncostatin m (OSM) is elevated in adipose tissue in conditions of obesity and type 2 diabetes in mice and humans, the aim of this study was to determine whether this cytokine plays a crucial role in the impairment of brown adipose tissue (BAT) activity and browning capacity that has been observed in people with obesity. Methods: C57BL/6J mice rendered obese by high-fat diet, their lean controls, and C57BL/6J mice fed a standard diet and implanted subcutaneously with a mini pump through a surgical procedure to deliver OSM or placebo were used. Preadipocytes or fully differentiated brown adipocytes were treated with OSM or vehicle with or without norepinephrine before harvesting. RNA was extracted and processed for qPCR analysis. Media from mature adipocytes was also collected to measure glycerol levels. Results: Studies demonstrated that OSM gene expression was increased in BAT of mice fed a high-fat diet. In addition, exogenous OSM impaired BAT activity and the browning capacity of white adipose tissue in vitro and in vivo. Conclusions: Overall, the results reveal a negative role for OSM on BAT and on the browning of white adipose tissue. Therefore, further studies are necessary to demonstrate whether OSM inhibition is a potential treatment for metabolic disorders.
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