ArticleClinical and translational medicine2025
Intestinal Fut2 deficiency exacerbated alcohol-related liver disease by disrupting nicotinamide metabolism.
Article in Clinical and translational medicine, 2025. 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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Who cites it
4 citing papers in PubMed.
- Intestinal neutral ceramidase exacerbates MASH pathogenesis.eGastroenterology · 2026Article
- FUT2-mediated intestinal fucosylation: a master regulator of host-microbiota symbiosis in health and disease.Frontiers in microbiology · 2026Review
- Intestinal neutral ceramidase, microbial metabolites and epithelial fucosylation in MASH.eGastroenterology · 2026Article
- Intestinal Fut2 deficiency exacerbated alcohol-related liver disease by disrupting nicotinamide metabolism.Clinical and translational medicine · 2025Article
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10 authors.
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Abstract
backgroundFucosyltransferase 2 (FUT2)-dependent fucosylation of intestinal epithelial cells is vital for preserving gut barrier integrity and microbial balance. Nevertheless, its precise involvement in alcohol-associated liver disease has yet to be fully elucidated.
methodsWe generated mice with intestinal epithelial cell-specific Fut2 knockout (Fut2
resultsThe loss of intestinal epithelial Fut2 exacerbates alcohol-related hepatic oxidative stress damage, and this effect is dependent on gut bacteria. A marked decrease in the abundance of bacteria carrying nicotinamidase (PncA) in the intestines of Fut2
conclusionThese findings reveal a gut microbiota-Fut2-pncA axis that modulates alcoholic liver injury in mice, which may offer insights into microbial contributions to alcoholic liver disease in people. KEY POINTS: Loss of intestinal epithelial fucosylation exacerbates alcohol-related liver injuries. Intestinal epithelial deletion of Fut2 disrupts nicotinamide (NAM) metabolism due to the decline in bacterial nicotinamidase (PncA). Supplemented with pncA overexpressed E.coli to restore gut PncA levels can improve liver damage in alcohol-induced intestinal epithelial Fut2 deletion mice.
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