ArticleCellular & molecular immunology2020
IL-29 promoted obesity-induced inflammation and insulin resistance.
Article in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 55 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Immunometabolic Dysregulation in Obesity: Integrating Macrophage Polarization, Metabolic Reprogramming, and Gut Microbiota Crosstalk.Immunity, inflammation and disease · 2026Review
- Serum profile of IL-29, IL-41, and raftlin in microvascular complications of type 2 diabetes mellitus.Scientific reports · 2026Article
- Altered Molecular Regulation of TUG Is a Central Feature of Insulin-Resistant Human Adipose Tissue.Diabetes · 2026Article
- Modeling fatty liver disease and progression with stem cell derived hepatocytes.Scientific reports · 2026Article
- L-Fucose alleviates inflammation, pyroptosis and mitochondrial injury in obesity-related cardiac injury via TLR4/MyD88/NF-κB pathway.Journal of translational medicine · 2025Article
- Cytokine concentration in peripheral blood of patients with childhood obesity.Frontiers in immunology · 2025Article
- The molecular interplay among gut dysbiosis, adipose tissue, and metabolite-derived damage-associated molecular patterns in metainflammation and atherogenesis.Frontiers in immunology · 2025Review
- Associations between type III interferons, obesity and clinical severity of COVID-19.Frontiers in immunology · 2025Article
- Interferon Upregulation Associates with Insulin Resistance in Humans.Current diabetes reviews · 2025Review
- Pulmonary Hypertension and Hyperglycemia-Not a Sweet Combination.Diagnostics (Basel, Switzerland) · 2024Review
- IL-33 regulates adipogenesis via Wnt/β-catenin/PPAR-γ signaling pathway in preadipocytes.Journal of translational medicine · 2024Article
- New treatment alternatives for primary and metastatic colorectal cancer by an integrated transcriptome and network analyses.Scientific reports · 2024Article
- Development and validation of a predictive model for severe white matter hyperintensity with obesity.Frontiers in aging neuroscience · 2024Article
- Interleukin-29 level in psoriasis before and after narrow-band ultraviolet B and its relationship with metabolic syndrome.Archives of dermatological research · 2023Article
- Low-grade inflammation is associated with a heterogeneous lipoprotein subclass profile in an apparently healthy population sample.Lipids in health and disease · 2023Article
- Review
- Lipedema: Insights into Morphology, Pathophysiology, and Challenges.Biomedicines · 2022Review
- 20 Years with SGBS cells - a versatile in vitro model of human adipocyte biology.International journal of obesity (2005) · 2022Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipocyte-macrophage crosstalk plays a critical role to regulate adipose tissue microenvironment and cause chronic inflammation in the pathogenesis of obesity. Interleukin-29 (IL-29), a member of type 3 interferon family, plays a role in host defenses against microbes, however, little is known about its role in metabolic disorders. We explored the function of IL-29 in the pathogenesis of obesity-induced inflammation and insulin resistance. We found that serum IL-29 level was significantly higher in obese patients. IL-29 upregulated IL-1β, IL-8, and monocyte chemoattractant protein-1 (MCP-1) expression and decreased glucose uptake and insulin sensitivity in human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes through reducing glucose transporter 4 (GLUT4) and AKT signals. In addition, IL-29 promoted monocyte/macrophage migration. Inhibition of IL-29 could reduce inflammatory cytokine production in macrophage-adipocyte coculture system, which mimic an obese microenvironment. In vivo, IL-29 reduced insulin sensitivity and increased the number of peritoneal macrophages in high-fat diet (HFD)-induced obese mice. IL-29 increased M1/M2 macrophage ratio and enhanced MCP-1 expression in adipose tissues of HFD mice. Therefore, we have identified a critical role of IL-29 in obesity-induced inflammation and insulin resistance, and we conclude that IL-29 may be a novel candidate target for treating obesity and insulin resistance in patients with metabolic disorders.
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Registered trials
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