ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Glucuronolactone Promotes Mucin Sulfation to Alleviate Deoxynivalenol-Induced Intestinal Injury via Microbiota-Dependent and -Independent AHR Activation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Deoxynivalenol (DON), a prevalent trichothecene mycotoxin, poses a global threat to the gut health of both humans and livestock. This study investigates the protective effects and underlying mechanisms of glucuronolactone (GLU) against DON-induced intestinal injury. In a piglet model, GLU effectively alleviated DON-induced intestinal injury and inflammation. Transcriptomic analysis revealed that GLU promotes mucin sulfation, a critical process for fortifying the intestinal mucus barrier. On the one hand, integrated microbiome and metabolomics analyses uncovered that GLU increased probiotic Lactobacillus amylovorus abundance and luminal indole-3-acetic acid level, thereby facilitating mucin sulfation. On the other hand, GLU itself directly boosted mucin sulfation in a microbiota-independent manner. Mechanistically, both the microbiota-dependent and -independent pathways through which GLU promoted mucin sulfation converged on the activation of aryl hydrocarbon receptor (AHR). Activated AHR transcriptionally up-regulated the expression of the sulfotransferase GAL3ST3, which drove mucin sulfation. This study identifies GLU as a promising nutritional intervention against DON-induced intestinal injury and reveals AHR-mediated mucin sulfation as a vital mechanism for maintaining intestinal barrier homeostasis.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.