ArticleFrontiers in endocrinology2024
From serum metabolites to the gut: revealing metabolic clues to susceptibility to subtypes of Crohn's disease and ulcerative colitis.
Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Metabolic Profiling of the Gut-Brain Axis in a Murine Model of Ulcerative Colitis with Raman Spectroscopy.ACS applied materials & interfaces · 2026Article
- Combined metabolomic and metagenomic analysis reveals inflammatory bowel disease diversity in pediatric and adult patients.World journal of gastroenterology · 2025Article
- Targeting FADS1-mediated lipid metabolism and signaling: a novel therapeutic strategy for precision oncology in colorectal and esophageal cancers.Cell death discovery · 2025Article
- Investigating Causal Links between Metabolite Profiles and Ulcerative Colitis: A Bidirectional Mendelian Randomization Study.Journal of medical signals and sensors · 2025Article
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14 authors.
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Abstract
Background and aims: Inflammatory bowel disease (IBD) is a common chronic inflammatory bowel disease characterized by diarrhea and abdominal pain. Recently human metabolites have been found to help explain the underlying biological mechanisms of diseases of the intestinal system, so we aimed to assess the causal relationship between human blood metabolites and susceptibility to IBD subtypes. Methods: We selected a genome-wide association study (GWAS) of 275 metabolites as the exposure factor, and the GWAS dataset of 10 IBD subtypes as the outcome, followed by univariate and multivariate analyses using a two-sample Mendelian randomization study (MR) to study the causal relationship between exposure and outcome, respectively. A series of sensitivity analyses were also performed to ensure the robustness of the results. Results: A total of 107 metabolites were found to be causally associated on univariate analysis after correcting for false discovery rate (FDR), and a total of 9 metabolites were found to be significantly causally associated on subsequent multivariate and sensitivity analyses. In addition we found causal associations between 7 metabolite pathways and 6 IBD subtypes. Conclusion: Our study confirms that blood metabolites and certain metabolic pathways are causally associated with the development of IBD subtypes and their parenteral manifestations. The exploration of the mechanisms of novel blood metabolites on IBD may provide new therapeutic ideas for IBD patients.
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