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Updated: Feb 19, 2026

An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
Published on: April 20, 2018
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.
Abstract:
Oncostatin M (OSM), a member of the IL-6 family of cytokines, plays an important role in various biologic actions, including cell growth, neuronal development, and inflammatory responses. Recently, we demonstrated the unique relationship between OSM and metabolic syndrome in mice. Mice lacking OSM receptor β subunit (OSMRβ-/- mice) exhibited late-onset obesity. Before the onset of obesity, adipose tissue inflammation and insulin resistance were observed in OSMRβ-/- mice. In addition, high-fat diet-induced metabolic disorders, including obesity, adipose tissue inflammation, insulin resistance, and hepatic steatosis, were aggravated in OSMRβ-/- mice compared to those in wild-type mice. Consistent with these findings, OSM treatment dramatically improved these metabolic disorders in the mouse model of metabolic syndrome. Interestingly, OSM directly changed the phenotypes of adipose tissue macrophages toward anti-inflammatory M2 type. Furthermore, fatty acid content in the hepatocytes was decreased by OSM through expression regulation of several key enzymes of hepatic lipid metabolism. These findings suggest that OSM is a novel therapeutic target for metabolic syndrome.
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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