<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen L</submitter><funding>Scientific Research Foundation of Wuhan Union Hospital</funding><funding>National Key R&amp;D Program of China</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Research and Development Program of China</funding><pagination>e70447</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12356993</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(8)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Fucosyltransferase 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.&lt;h4>Methods&lt;/h4>We generated mice with intestinal epithelial cell-specific Fut2 knockout (Fut2&lt;sup>△IEC&lt;/sup>) and established a chronic-binge alcohol model. 16S rRNA sequencing and metabolomics analysis were used to reveal differences in the composition and function of faecal bacteria.&lt;h4>Results&lt;/h4>The 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</pubmed_abstract><journal>Clinical and translational medicine</journal><pubmed_title>Intestinal Fut2 deficiency exacerbated alcohol-related liver disease by disrupting nicotinamide metabolism.</pubmed_title><pmcid>PMC12356993</pmcid><funding_grant_id>2023XHYN019</funding_grant_id><funding_grant_id>82000561</funding_grant_id><funding_grant_id>2022YFA1305600</funding_grant_id><funding_grant_id>81974062</funding_grant_id><funding_grant_id>82400652</funding_grant_id><funding_grant_id>82274314</funding_grant_id><funding_grant_id>82100375</funding_grant_id><funding_grant_id>82470584</funding_grant_id><pubmed_authors>Shang L</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Chu H</pubmed_authors><pubmed_authors>Gao W</pubmed_authors><pubmed_authors>Yuan H</pubmed_authors><pubmed_authors>Hou X</pubmed_authors><pubmed_authors>Yang S</pubmed_authors><pubmed_authors>Yin Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Intestinal Fut2 deficiency exacerbated alcohol-related liver disease by disrupting nicotinamide metabolism.</name><description>&lt;h4>Background&lt;/h4>Fucosyltransferase 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.&lt;h4>Methods&lt;/h4>We generated mice with intestinal epithelial cell-specific Fut2 knockout (Fut2&lt;sup>△IEC&lt;/sup>) and established a chronic-binge alcohol model. 16S rRNA sequencing and metabolomics analysis were used to reveal differences in the composition and function of faecal bacteria.&lt;h4>Results&lt;/h4>The 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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-05-01T18:43:32.261Z</modification><creation>2026-04-07T17:09:19.828Z</creation></dates><accession>S-EPMC12356993</accession><cross_references><pubmed>40817598</pubmed><doi>10.1002/ctm2.70447</doi></cross_references></HashMap>