ArticleMedicine2025
The role of gut microbiota and plasma metabolites in ulcerative colitis: Insights from Mendelian randomization analysis.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Metabolic Disorders and Inflammatory Bowel Diseases: Unraveling Shared Pathways and Clinical Interactions.Metabolites · 2026Review
- Mechanism and application ofFrontiers in cellular and infection microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging research suggests that alterations in gut microbiota composition may play a significant role in the pathogenesis of ulcerative colitis (UC). Plasma metabolites, which are influenced by gut microbiota, have also been implicated, but their role in UC remains unclear. This study aims to determine whether specific plasma metabolites mediate the causal relationship between gut microbiota and UC using Mendelian randomization (MR) analysis. This study employed publicly available summary-level data from genome-wide association studies and metagenomic datasets. Gut microbiota data were derived from the FINRISK cohort (5959 participants), plasma metabolite data from the Canadian Longitudinal Study on Aging (8299 individuals), and UC data from multiple consortia (17,030 cases and 883,787 controls). Forward and reverse MR analyses, supplemented by linkage disequilibrium score regression (LDSC), were conducted to assess causal relationships. Mediation effects of plasma metabolites between gut microbiota and UC were analyzed using the product of coefficients method. Various sensitivity analyses, including MR-Egger and MR-PRESSO, were applied to detect pleiotropy and ensure robust results. The study identified 20 bacterial taxa and 93 plasma metabolites linked to UC. Forward MR analysis showed that Clostridium S felsineum increased UC risk via reduced carnitine levels, with a mediation proportion of 39.77%. Eubacterium callanderi was associated with decreased UC risk through the tryptophan to pyruvate ratio (16.02% mediation). Additionally, species CAG-590 sp000431135 increased UC risk through elevated mannitol/sorbitol levels, mediating 28.38% of the effect. Sensitivity analyses confirmed the robustness of these findings, with minimal heterogeneity and pleiotropy detected. This study highlights the significant role of gut microbiota and their associated plasma metabolites in the pathogenesis of UC. Specific microbial species influence UC through metabolites, suggesting potential therapeutic targets. Modulating carnitine, tryptophan metabolism, or sugar alcohols could offer promising avenues for UC management.
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Registered trials
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