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To induce steatosis, female C57BL\/6J mice were pair\u2010fed with a liquid control diet (C) or a fat\u2010, fructose\u2010 and cholesterol\u2010rich diet (FFC) for 8\u00a0weeks. Mice received the diets \u00b1 2.49\u00a0g L\u2010arginine\/kg bw\/day for additional 5\u00a0weeks. Furthermore, mice fed C or FFC \u00b1 L\u2010arginine\/kg bw\/day for 8\u00a0weeks were concomitantly treated with the arginase inhibitor N<jats:sup>\u03c9<\/jats:sup>\u2010hydroxy\u2010nor\u2010L\u2010arginine (nor\u2010NOHA, 0.01\u00a0g\/kg bw). Liver damage, intestinal barrier function, nitric oxide levels and arginase activity in small intestine were assessed. Also, arginase activity was measured in serum from 13 patients with steatosis (NAFL) and 14 controls. The development of steatosis with beginning inflammation was associated with impaired intestinal barrier function, increased nitric oxide levels and a loss of arginase activity in small intestine in mice. L\u2010arginine supplementation abolished the latter along with an improvement of intestinal barrier dysfunction; nor\u2010NOHA attenuated these effects. In patients with NAFL, arginase activity in serum was significantly lower than in healthy controls. Our data suggest that increased formation of nitric oxide and a loss of intestinal arginase activity is critical in NAFLD\u2010associated intestinal barrier dysfunction.<\/jats:p>","DOI":"10.1111\/jcmm.17175","type":"journal-article","created":{"date-parts":[[2022,1,14]],"date-time":"2022-01-14T08:40:24Z","timestamp":1642149624000},"page":"1206-1218","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Alterations of nitric oxide homeostasis as trigger of intestinal barrier dysfunction in non\u2010alcoholic fatty liver disease"],"prefix":"10.1111","volume":"26","author":[{"given":"Anja","family":"Baumann","sequence":"first","affiliation":[{"name":"Department of Nutritional Sciences Molecular Nutritional Science University of Vienna Vienna 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