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Relative to an ad libitum chow-fed group, the high-fat-fed controls had three- to fourfold greater expression of fatty acid transporter CD36 mRNA and developed mild steatosis but little other hepatic pathology. NAC treatment resulted in increased somatic growth relative to controls (4.0 \u00b1 0.1 vs. 3.1 \u00b1 0.1 g\/day) and increased hepatic steatosis score (3.5 \u00b1 0.6 vs. 2.7 \u00b1 1.2), associated with suppression of the triglyceride hydrolyzing protein adiponutrin, but produced no elevation in serum alanine aminotransferase (ALT). Chronic EtOH treatment increased expression of fatty acid transport protein FATP-2 mRNA twofold, resulting in marked hepatic steatosis, oxidative stress, and a twofold elevation in serum ALT. However, no changes in tumor necrosis factor-\u03b1 or transforming growth factor-\u03b2 expression were observed. Fibrosis, as measured by Masson's trichrome and picrosirius red staining, and a twofold increase in expression of type I and type III collagen mRNA, was only observed after EtOH treatment. Long-term EtOH treatment increased hepatocyte proliferation but did not modify the hepatic mRNAs for hedgehog pathway ligands or target genes or genes regulating epithelial-to-mesenchymal transition. Although the effects of NAC on EtOH-induced fibrosis could not be fully evaluated, NAC had additive effects on hepatocyte proliferation and prevented EtOH-induced oxidative stress and necrosis, despite a failure to reverse hepatic steatosis.<\/jats:p>","DOI":"10.1152\/ajpgi.00145.2010","type":"journal-article","created":{"date-parts":[[2010,11,5]],"date-time":"2010-11-05T02:10:30Z","timestamp":1288923030000},"page":"G109-G119","source":"Crossref","is-referenced-by-count":30,"title":["Effects of long-term ethanol administration in a rat total enteral nutrition model of alcoholic liver disease"],"prefix":"10.1152","volume":"300","author":[{"given":"Martin J. 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