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Oncostatin m impairs brown adipose tissue thermogenic function and the browning of subcutaneous white adipose tissue
David Sánchez-Infantes1, Rubén Cereijo2,3,4, Marion Peyrou2,3,4
1Department of Endocrinology and Nutrition, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol, Barcelona, Spain.
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.
Insights
Oncostatin M (OSM) negatively impacts brown adipose tissue (BAT) activity and browning in obesity. This suggests OSM inhibition could be a potential therapeutic strategy for metabolic disorders.
Area of Science:
- Metabolic research
- Adipose tissue biology
- Cytokine signaling
Background:
- Oncostatin M (OSM) is elevated in adipose tissue during obesity and type 2 diabetes.
- Obesity is associated with impaired brown adipose tissue (BAT) activity and browning capacity.
Purpose of the Study:
- To investigate the role of Oncostatin M (OSM) in the dysfunction of brown adipose tissue (BAT) observed in obesity.
- To determine if OSM contributes to the reduced activity and browning potential of BAT in obese individuals.
Main Methods:
- Obese and lean mice models, including high-fat diet-induced obesity.
- In vitro studies using preadipocytes and brown adipocytes treated with OSM and norepinephrine.
- Gene expression analysis (qPCR) and measurement of glycerol release from adipocytes.
Main Results:
- OSM gene expression was significantly increased in the BAT of mice fed a high-fat diet.
- Exogenous administration of OSM impaired BAT activity and the capacity for white adipose tissue browning, both in vitro and in vivo.
Conclusions:
- Oncostatin M (OSM) plays a detrimental role in brown adipose tissue (BAT) function and white adipose tissue browning.
- Further research is warranted to explore OSM inhibition as a potential therapeutic approach for metabolic disorders.
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