ArticleNature metabolism2021
Inhibition of the IL-17A axis in adipocytes suppresses diet-induced obesity and metabolic disorders in mice.
Article in Nature metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05162001 (Body Weight Response With Disulfiram in Humans. Concept Testing Study), which is not on this map. Cited by 53 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Body Weight Response With Disulfiram in Humans. Concept Testing Study
Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- Metabolic Complications in Autoimmune and Autoinflammatory Diseases: Pathophysiology, Clinical Implications, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- FXR-YAP signalling maintains biliary epithelial cell identity and preserves liver homeostasis.Nature metabolism · 2026Article
- The obesity-inflammation axis in psoriatic disease: mechanisms and therapeutic strategies.Nature reviews. Rheumatology · 2026Review
- USP25 deficiency suppresses diet-induced obesity via ubiquitination and degradation of PARP1 and Elovl3 downregulation.Journal of lipid research · 2026Article
- Digoxin attenuates LPS-induced acute lung injury in mice via NF-κB and HIF-1α inhibition.Biomolecules & biomedicine · 2026Article
- Advances in the Role of Adipose Tissue in Promoting Injury Repair and Resist Infection.Immunity, inflammation and disease · 2026Review
- Targeting IL-17 Presents a Promising Strategy for Treating Diseases Related to the Dysregulation of Lipid Homeostasis.Mediators of inflammation · 2026Review
- Beyond inflammation: metabolic implications of biological and TsDMARD therapies in dermatologic and rheumatologic diseases.Frontiers in immunology · 2026Review
- CDK5 regulates PPARγ/NF-κB signaling to exacerbate obesity-related osteoarthritis via modulating macrophage polarization and chondrocyte apoptosis.Cellular & molecular biology letters · 2025Article
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- From fat storage to immune hubs: the emerging role of adipocytes in coordinating the immune response to infection.The FEBS journal · 2025Review
- Immune Regulatory Crosstalk in Adipose Tissue Thermogenesis.Comprehensive Physiology · 2025Review
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- Multi-omics landscape of childhood simple obesity: novel insights into pathogenesis and biomarkers discovery.Cell & bioscience · 2024Article
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- Exploring the Antidiabetic Potential ofPlants (Basel, Switzerland) · 2024Article
- Targeting osteoblastic 11β-HSD1 to combat high-fat diet-induced bone loss and obesity.Nature communications · 2024Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overnutrition causes obesity, a global health problem without any effective therapy. Obesity is characterized by low-grade inflammation, which predisposes individuals to metabolic syndrome via unknown mechanisms. Here, we demonstrate that abolishing the interleukin-17A (IL-17A) axis in mice by inhibition of RORγt-mediated IL-17A production by digoxin, or by ubiquitous deletion of IL-17 receptor A (Il17ra), suppresses diet-induced obesity (DIO) and metabolic disorders, and promotes adipose-tissue browning, thermogenesis and energy expenditure. Genetic ablation of Il17ra specifically in adipocytes is sufficient to completely prevent DIO and metabolic dysfunction in mice. IL-17A produced in response to DIO induces PPARγ phosphorylation at Ser273 in adipocytes in a CDK5-dependent manner, thereby modifying expression of diabetogenic and obesity genes, which correlates with IL-17A signalling in white adipose tissues of individuals with morbid obesity. These findings reveal an unanticipated role for IL-17A in adipocyte biology, in which its direct action pathogenically reprograms adipocytes, promoting DIO and metabolic syndrome. Targeting the IL-17A axis could be an efficient antiobesity strategy.
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