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

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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.

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Acknowledgements

This work was supported by a Grant-in-Aid for Scientific Research (B) (JSPS KAKENHI Grant number 26282195) from the Japan Society for the Promotion of Science, Research Grant on Priority Areas from Wakayama Medical University, and the 2012 Wakayama Medical Award for Young Researchers.

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Correspondence to Tadasuke Komori.

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Komori, T., Morikawa, Y. Oncostatin M in the development of metabolic syndrome and its potential as a novel therapeutic target. Anat Sci Int 93, 169–176 (2018). https://doi.org/10.1007/s12565-017-0421-y

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