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Title: A role for Oncostatin M in the impairment of glucose homeostasis in obesity
Author: Piquer García, Irene
Campderrós Traver, Laura
Taxerås, Siri D.
Gavaldà i Navarro, Aleix
Pardo, Rosario
Vila, María
Pellitero, Silvia
Martínez, Eva
Tarascó, Jordi
Moreno, Pau
Villarroya i Terrade, Joan
Cereijo Téllez, Rubén
González, Lorena
Reyes, Majorie
Rodriguez-Fernández, Silvia
Vives-Pi, Marta
Lerin, Carles
Elks, Carrie M.
Stephens, Jacqueline M.
Puig Domingo, Manuel
Villarroya i Gombau, Francesc
Villena, Josep A.
Sánchez-Infantes, David
Keywords: Obesitat
Issue Date: 13-Oct-2019
Publisher: Endocrine Society
Abstract: CONTEXT: Oncostatin M (OSM) plays a key role in inflammation, but its regulation and function during obesity is not fully understood. OBJECTIVE: The aim of this study was to evaluate the relationship of OSM with the inflammatory state that leads to impaired glucose homeostasis in obesity. We also assessed whether OSM immunoneutralization could revert metabolic disturbances caused by a high-fat diet (HFD) in mice. DESIGN: 28 patients with severe obesity were included and stratified into two groups: (1) glucose levels <100 mg/dL and (2) glucose levels >100 mg/dL. White adipose tissue was obtained to examine OSM gene expression. Human adipocytes were used to evaluate the effect of OSM in the inflammatory response, and HFD-fed C57BL/6J mice were injected with anti-OSM antibody to evaluate its effects. RESULTS: OSM expression was elevated in subcutaneous and visceral fat from patients with obesity and hyperglycemia, and correlated with Glut4 mRNA levels, serum insulin, homeostatic model assessment of insulin resistance, and inflammatory markers. OSM inhibited adipogenesis and induced inflammation in human adipocytes. Finally, OSM receptor knockout mice had increased Glut4 mRNA levels in adipose tissue, and OSM immunoneutralization resulted in a reduction of glucose levels and Ccl2 expression in adipose tissue from HFD-fed mice. CONCLUSIONS: OSM contributes to the inflammatory state during obesity and may be involved in the development of insulin resistance.
Note: Versió postprint del document publicat a:
It is part of: Journal of Clinical Endocrinology & Metabolism, 2019, vol. 105, num. 3
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ISSN: 0021-972X
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

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