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Oncostatin m impairs brown adipose tissue thermogenic function and the browning of subcutaneous white adipose tissue
Author(s) -
SánchezInfantes David,
Cereijo Rubén,
Peyrou Marion,
PiquerGarcia Irene,
Stephens Jacqueline M.,
Villarroya Francesc
Publication year - 2017
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21679
Subject(s) - white adipose tissue , oncostatin m , adipose tissue , browning , brown adipose tissue , endocrinology , medicine , adipose tissue macrophages , adipocyte , chemistry , cytokine , interleukin 6 , biochemistry
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.