Oncostatin M tied to impaired glucose homeostasis in obesity
An association exists between oncostatin M (OSM) and the inflammatory state during obesity, which may lead to the development of insulin resistance, reveals a study.
The authors included 28 patients with severe obesity and stratified them into two groups: (1) glucose levels <100 mg/dL and (2) glucose levels >100 mg/dL. They also examined OSM gene expression by obtaining white adipose tissue.
In addition, the authors also determined whether OSM immunoneutralization could revert metabolic disturbances caused by a high-fat diet (HFD) in mice. Human adipocytes were used to examine the effect of OSM in the inflammatory response, while HFD-fed C57BL/6J mice were injected with anti-OSM antibody to assess its effects.
Patients with obesity and hyperglycaemia showed an elevated OSM expression in subcutaneous and visceral fat. Moreover, OSM expression was shown to have an association with Glut4 mRNA levels, serum insulin, homeostatic model assessment of insulin resistance and inflammatory markers. OSM also inhibited adipogenesis and induced inflammation in human adipocytes.
Furthermore, OSM receptor knockout mice showed elevated levels of Glut4 mRNA in adipose tissue. OSM immunoneutralization led to a decrease in glucose levels as well as Ccl2 expression in adipose tissue from HFD-fed mice.
“OSM contributes to the inflammatory state during obesity and may be involved in the development of insulin resistance,” the authors said.
An early study reported that adipocyte OSM receptor β signaling is involved in the regulation of adipose tissue homeostasis. Additionally, in obesity, OSM receptor β ablation promotes adipose tissue inflammation, which worsens insulin resistance. [J Biol Chem 2016;291:17066-17076]