{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T17:49:58Z","timestamp":1787593798635,"version":"build-2736575974"},"reference-count":41,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,8,2]],"date-time":"2020-08-02T00:00:00Z","timestamp":1596326400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003398","name":"Shanxi Scholarship Council of China","doi-asserted-by":"publisher","award":["20161625"],"award-info":[{"award-number":["20161625"]}],"id":[{"id":"10.13039\/501100003398","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AA020864"],"award-info":[{"award-number":["R01 AA020864"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AA24726, R01AA020703, U01 AA026939, P30 DK1205"],"award-info":[{"award-number":["R01 AA24726, R01AA020703, U01 AA026939, P30 DK1205"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Fucosyltransferase 2 (Fut2)\u2010mediated intestinal \u03b11\u20102\u2010fucosylation is important in maintaining a symbiotic host\u2013microbiota relationship and can protect against several pathogens. Intestinal dysbiosis is an important factor for the progression of experimental ethanol (EtOH)\u2010induced liver disease, but the role of Fut2 in modulating the intestinal glycocalyx during alcohol\u2010associated liver disease is unknown. We investigated the role of Fut2\u2010mediated intestinal \u03b11\u20102\u2010fucosylation for the development of alcohol\u2010associated liver disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Immunohistochemistry staining was applied to evaluate \u03b11\u20102\u2010fucosylation in duodenal biopsies from patients with alcohol use disorder. Wild\u2010type (WT) and\n                      <jats:italic>Fut2<\/jats:italic>\n                      \u2010deficient littermate mice were subjected to Lieber\u2013DeCarli models of chronic EtOH administration and the chronic\u2010binge EtOH diet (NIAAA model).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Intestinal \u03b11\u20102\u2010fucosylation was down\u2010regulated in patients with alcohol use disorder. Lack of \u03b11\u20102\u2010fucosylation in\n                      <jats:italic>Fut2<\/jats:italic>\n                      \u2010deficient mice exacerbates chronic EtOH\u2010induced liver injury, steatosis, and inflammation without affecting EtOH metabolism. Dietary supplementation of the \u03b11\u20102\u2010fucosylated glycan 2\u2032\u2010fucosyllactose (2\u2032\u2010FL) ameliorates EtOH\u2010induced liver disease in\n                      <jats:italic>Fut2\u2010<\/jats:italic>\n                      deficient mice in the NIAAA model. Despite no direct effects on growth of\n                      <jats:italic>Enterococcus faecalis<\/jats:italic>\n                      in vitro, intestinal \u03b11\u20102\u2010fucosylation reduces colonization of cytolysin\u2010positive\n                      <jats:italic>E. faecalis<\/jats:italic>\n                      in the intestine of EtOH\u2010fed mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Intestinal \u03b11\u20102\u2010fucosylation acts as a host\u2010protective mechanism against EtOH\u2010induced liver disease. 2\u2032\u2010FL is an oligosaccharide naturally present in human milk that could be considered as therapeutic agent for alcohol\u2010associated liver disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.14405","type":"journal-article","created":{"date-parts":[[2020,7,6]],"date-time":"2020-07-06T15:27:05Z","timestamp":1594049225000},"page":"1842-1851","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Deficiency of Intestinal \u03b11\u20102\u2010Fucosylation Exacerbates Ethanol\u2010Induced Liver Disease in Mice"],"prefix":"10.1111","volume":"44","author":[{"given":"Rongrong","family":"Zhou","sequence":"first","affiliation":[{"name":"From the Department of Infectious Diseases Key Laboratory of Viral Hepatitis Xiangya Hospital Central South University Changsha China"},{"name":"Department of Medicine University of California San Diego La Jolla California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Llorente","sequence":"additional","affiliation":[{"name":"Department of Medicine University of California San Diego La Jolla California 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