ArticleFrontiers in microbiology2026
Integrative analysis of gut microbiota, plasma metabolome, and gene expression identifies causal mediators in Graves' disease pathogenesis.
Article in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Graves' disease (GD) is characterized by hyperthyroidism and is influenced by genetic and environmental factors. The "gut-thyroid axis" establishes a connection between the gut microbiota and GD, yet the underlying potential mechanisms remain unclear. This study employed Mendelian randomization to investigate the causal relationships between the gut microbiota and GD, aiming to identify key microbial taxa and their metabolites, as well as to explore the regulatory roles of relevant genes in the pathogenesis of GD. Methods: We utilized the two-sample Mendelian randomization (MR) approach to evaluate the causal effects of gut microbiota and plasma metabolites on GD. Mediation analysis was conducted to explore the associations of metabolites in linking gut microbiota to GD. Additionally, we employed bioinformatics tools to identify GD-regulating genes within the gut microbiome and validated their expression levels in peripheral blood mononuclear cells from GD mouse models. Results: Mendelian randomization analysis identified eight gut microbes associated with GD, six of which were positively correlated with an increased risk, while two were negatively correlated. Additionally, 56 plasma metabolites exhibited potential causal relationships with GD; of these, 27 were positively associated with risk and 29 were negatively associated. Mediation analysis revealed that three bacteria influenced GD through five plasma metabolites. Specifically, the mannose to glycerol ratio and 1-(1-enyl-palmitoyl)-GPC (p-16:0) mediated the effect of Conclusion: This study reveals that the composition of gut microbiota and its related metabolites promote the development of GD through the modulation of gene expression in peripheral blood mononuclear cells. Our findings have significant implications for the advancement of gut microbiota-based diagnostic techniques and targeted therapies for GD.
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