Oncostatin M in the development of metabolic syndrome and its potential as a novel therapeutic target

Tadasuke Komori1, Yoshihiro Morikawa2

  • 1Department of Anatomy and Neurobiology, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan. tadasuke@wakayama-med.ac.jp.

Insights

Oncostatin M (OSM) deficiency worsens metabolic syndrome in mice. OSM treatment improved obesity, inflammation, and insulin resistance, suggesting OSM as a therapeutic target.

Area of Science:

  • Immunology
  • Metabolism
  • Endocrinology

Background:

  • Oncostatin M (OSM), an IL-6 family cytokine, influences cell growth, development, and inflammation.
  • A link between OSM and metabolic syndrome in mice has been recently identified.

Purpose of the Study:

  • To investigate the role of OSM in metabolic syndrome.
  • To evaluate OSM as a potential therapeutic target for metabolic disorders.

Main Methods:

  • Utilized OSMRβ knockout mice to study OSM deficiency effects.
  • Administered OSM treatment to mice with diet-induced metabolic disorders.
  • Analyzed adipose tissue inflammation, insulin resistance, and hepatic steatosis.
  • Assessed macrophage phenotype and hepatic lipid metabolism gene expression.

Main Results:

  • OSMRβ knockout mice developed late-onset obesity, adipose tissue inflammation, and insulin resistance.
  • High-fat diet exacerbated metabolic disorders in OSMRβ knockout mice.
  • OSM treatment ameliorated obesity, adipose tissue inflammation, insulin resistance, and hepatic steatosis.
  • OSM shifted adipose tissue macrophages to an anti-inflammatory M2 phenotype.
  • OSM reduced hepatic fatty acid content by regulating lipid metabolism enzymes.

Conclusions:

  • OSM plays a protective role against metabolic syndrome development and progression.
  • OSM demonstrates therapeutic potential for treating metabolic syndrome.
  • Targeting OSM may offer a novel strategy for managing metabolic disorders.

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