ArticleThe Journal of biological chemistry2014
Deficiency of oncostatin M receptor β (OSMRβ) exacerbates high-fat diet-induced obesity and related metabolic disorders in mice.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- The Role of the OSM/OSMRβ Axis in Chronic Liver Disease Progression and Hepatocellular Carcinoma Development: A Focus on MASLD/MASH.International journal of molecular sciences · 2026Review
- Immunotherapy drug target identification using machine learning and patient-derived tumour explant validation.Nature machine intelligence · 2026Article
- Differential chromatin accessibility and Gene Expression Associated with Backfat Deposition in pigs.BMC genomics · 2024Article
- Article
- Macrophage-derived Osteopontin (SPP1) Protects From Nonalcoholic Steatohepatitis.Gastroenterology · 2023Article
- OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling.Journal of translational medicine · 2023Article
- Oncostatin M promotes lipolysis in white adipocytes.Adipocyte · 2022Article
- Oncostatin M Induces Lipolysis and Suppresses Insulin Response in 3T3-L1 Adipocytes.International journal of molecular sciences · 2022Article
- New insights into IL-6 family cytokines in metabolism, hepatology and gastroenterology.Nature reviews. Gastroenterology & hepatology · 2021Review
- Essential roles of oncostatin M receptor β signaling in renal crystal formation in mice.Scientific reports · 2020Article
- A Role for Oncostatin M in the Impairment of Glucose Homeostasis in Obesity.The Journal of clinical endocrinology and metabolism · 2020Article
- Adipocyte Oncostatin Receptor Regulates Adipose Tissue Homeostasis and Inflammation.Frontiers in immunology · 2020Review
- Clcn3 deficiency ameliorates high-fat diet-induced obesity and adipose tissue macrophage inflammation in mice.Acta pharmacologica Sinica · 2019Article
- LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway.Journal of cellular physiology · 2019Article
- Review: the Roles and Mechanisms of Glycoprotein 130 Cytokines in the Regulation of Adipocyte Biological Function.Inflammation · 2019Review
- Article
- Oncostatin M, an Underestimated Player in the Central Nervous System.Frontiers in immunology · 2019Review
- Cachexia-associated adipose loss induced by tumor-secreted leukemia inhibitory factor is counterbalanced by decreased leptin.JCI insight · 2018Article
- Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor-neutralizing therapy in patients with inflammatory bowel disease.Nature medicine · 2017Article
- Oncostatin M receptor β deficiency attenuates atherogenesis by inhibiting JAK2/STAT3 signaling in macrophages.Journal of lipid research · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncostatin M (OSM) belongs to the IL-6 family of cytokines and has diverse biological effects, including the modulation of inflammatory responses. In the present study we analyzed the roles of OSM signaling in obesity and related metabolic disorders. Under a high-fat diet condition, OSM receptor β subunit-deficient (OSMRβ(-/-)) mice exhibited increases in body weight and food intake compared with those observed in WT mice. In addition, adipose tissue inflammation, insulin resistance, and hepatic steatosis were more severe in OSMRβ(-/-) mice than in wild-type (WT) mice. These metabolic phenotypes did not improve when OSMRβ(-/-) mice were pair-fed with WT mice, suggesting that the effects of OSM signaling on these phenotypes are independent of the increases in the body weight and food intake. In the liver of OSMRβ(-/-) mice, the insulin-induced phosphorylation of p70 S6 kinase remained intact, whereas insulin-induced FOXO1 phosphorylation was impaired. In addition, OSMRβ(-/-) mice displayed a higher expression of genes related to de novo lipogenesis in the liver than WT mice. Furthermore, treatment of genetically obese ob/ob mice with OSM improved insulin resistance, adipose tissue inflammation, and hepatic steatosis. Intraportal administration of OSM into ob/ob mice activated STAT3 and increased the expression of long-chain acyl-CoA synthetase (ACSL) 3 and ACSL5 with decreased expression of fatty acid synthase in the liver, suggesting that OSM directly induces lipolysis and suppresses lipogenesis in the liver of obese mice. These findings suggest that defects in OSM signaling promote the deterioration of high-fat diet-induced obesity and related metabolic disorders.
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