ArticleInvestigative ophthalmology & visual science2025
Butyrate Ameliorates Graves' Orbitopathy Through Regulating Orbital Fibroblast Phenotypes and Gut Microbiota.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Gut Microbial Metabolite Indole-3-Acetic Acid Exerts Protective Effects by Regulating Orbital Fibroblast Fibrosis in Thyroid Eye Disease.Investigative ophthalmology & visual science · 2026Article
- A bispecific-aptamer TSHR-CD80-1 treats thyroid eye disease by inhibiting CD8Cell communication and signaling : CCS · 2026Article
- Association of a Novel Dietary Index Assessing Gut Microbiota Impact With Rheumatoid Arthritis: A Nationwide Population-Based Study.Food science & nutrition · 2026Article
- Gut microbiota and its metabolites with thyroid diseases: functions and mechanisms.Frontiers in immunology · 2026Review
- The role of gut microbiota in autoimmune thyroid diseases: nutritional determinants and diet-based modulation.Frontiers in endocrinology · 2026Review
- Gut microbiota in asthma: mechanisms, clinical evidence, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Unravelling the pathogenic mechanisms in Graves' orbitopathy.European thyroid journal · 2025Review
- Epac1 Inhibits Orbital Fibroblast Activation to Ameliorate Thyroid-Associated Orbitopathy-Like Features Through the JAK/STAT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
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Authors and funding
8 authors.
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Abstract
Purpose: Graves' orbitopathy (GO), the common extrathyroidal complication of Graves' disease (GD), is characterized by orbital fibroblast stimulation, adipogenesis, and hyaluronan production. Recently, gut microbiota and its metabolites have garnered attention for their possible involvement in GO. Methods: This study utilized an animal model of GO and examined the effects of butyrate treatment on orbital fibroblast cells and gut microbiota. Ex vivo experiments were performed using orbital fibroblasts derived from healthy patients' and patients' with GO orbital tissue to evaluate vitality, activation, and adipogenesis in response to butyrate treatment. Gut microbiota diversity was also analyzed in butyrate-treated and untreated GO mice. Results: In human orbital fibroblasts, butyrate treatment dramatically decreased the vitality of GO-derived fibroblasts without harming normal fibroblasts. Butyrate prevented activation and fibrotic processes induced by transforming growth factor beta 1 (TGF-β1) in GO and normal fibroblasts. Additionally, butyrate reduced lipid droplet formation and downregulated lipogenic markers in GO and normal orbital fibroblasts, inhibiting adipogenesis. In the GO mouse model, butyrate therapy improved orbital histological abnormalities and normalized serum thyroid hormone and antibody levels. The intestinal microbiome of butyrate-treated GO mice also changed significantly, with a reduction in certain bacteria (Bifidobacterium, GCA-900066575, and Parabacteroides) and an increase in others (Bacteroides and Rikenellaceae_RC9). Conclusions: Butyrate ameliorates several of the symptoms of GO, lowering GO orbital fibroblast viability, adipogenesis, and TGF-β1-induced fibrosis without damaging normal fibroblasts. Butyrate normalizes thyroid function in a GO mouse model, improves histopathological alterations, and transforms gut microbiota populations, proving its potential in treating GO through the gut-thyroid axis.
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