David Sánchez-Infantes1, Rubén Cereijo2,3,4, Marion Peyrou2,3,4, Irene Piquer-Garcia1, Jacqueline M Stephens5, Francesc Villarroya2,3,4. 1. Department of Endocrinology and Nutrition, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol, Barcelona, Spain. 2. Department of Biochemistry and Molecular Biology, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain. 3. Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición (CIBEROBN), ISCIII, Madrid, Spain. 4. Institut de Recerca Pediàtrica Hospital Sant Joan de Déu (IRP-HSJD) University of Barcelona, Barcelona, Spain. 5. Department of Biological Science, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, USA.
Abstract
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.
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.
Authors: S Pellitero; I Piquer-Garcia; G Ferrer-Curriu; R Puig; E Martínez; P Moreno; J Tarascó; J Balibrea; C Lerin; M Puig-Domingo; F Villarroya; A Planavila; D Sánchez-Infantes Journal: Int J Obes (Lond) Date: 2017-10-30 Impact factor: 5.095