ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Effects of long-term ethanol administration in a rat total enteral nutrition model of alcoholic liver disease.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Pathogenesis of Alcohol-Associated Fatty Liver: Lessons From Transgenic Mice.Frontiers in physiology · 2022Review
- Natural Compounds: A Potential Treatment for Alcoholic Liver Disease?Frontiers in pharmacology · 2021Review
- Alcohol effects on hepatic lipid metabolism.Journal of lipid research · 2020Review
- Effect of ethanol on lipid metabolism.Journal of hepatology · 2019Review
- Impacts of WNT1-inducible signaling pathway protein 1 polymorphism on hepatocellular carcinoma development.PloS one · 2018Article
- Anti-steatotic and anti-fibrotic effects of the KCa3.1 channel inhibitor, Senicapoc, in non-alcoholic liver disease.World journal of gastroenterology · 2017Article
- Soy protein isolate inhibits hepatic tumor promotion in mice fed a high-fat liquid diet.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- Soy Protein Isolate Protects Against Ethanol-Mediated Tumor Progression in Diethylnitrosamine-Treated Male Mice.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Article
- Increased 4-hydroxynonenal protein adducts in male GSTA4-4/PPAR-α double knockout mice enhance injury during early stages of alcoholic liver disease.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Alcohol consumption, Wnt/β-catenin signaling, and hepatocarcinogenesis.Advances in experimental medicine and biology · 2015Review
- N-acetylcysteine inhibits the up-regulation of mitochondrial biogenesis genes in livers from rats fed ethanol chronically.Alcoholism, clinical and experimental research · 2014Article
- Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/β-catenin signaling pathway.Cancer prevention research (Philadelphia, Pa.) · 2014Article
- Influence of fat/carbohydrate ratio on progression of fatty liver disease and on development of osteopenia in male rats fed alcohol via total enteral nutrition (TEN).Alcohol (Fayetteville, N.Y.) · 2014Article
- Increased dietary fat contributes to dysregulation of the LKB1/AMPK pathway and increased damage in a mouse model of early-stage ethanol-mediated steatosis.The Journal of nutritional biochemistry · 2013Article
- Susceptibility of L-FABP-/- mice to oxidative stress in early-stage alcoholic liver.Journal of lipid research · 2013Article
- N-acetylcysteine (NAC) diminishes the severity of PCB 126-induced fatty liver in male rodents.Toxicology · 2012Article
- β-catenin is essential for ethanol metabolism and protection against alcohol-mediated liver steatosis in mice.Hepatology (Baltimore, Md.) · 2012Article
- Oxidative Stress and the ER Stress Response in a Murine Model for Early-Stage Alcoholic Liver Disease.Journal of toxicology · 2012Article
- Glutathione and Transsulfuration in Alcohol-Associated Tissue Injury and Carcinogenesis.Advances in experimental medicine and biologyReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Male Sprague-Dawley rats were chronically fed a high-unsaturated-fat diet for 130 days by using total enteral nutrition (TEN), or the same diet in which ethanol (EtOH) isocalorically replaced carbohydrate calories. Additional groups were supplemented with the antioxidant N-acetylcysteine (NAC) at 1.7 g·kg(-1)·day(-1). 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 ± 0.1 vs. 3.1 ± 0.1 g/day) and increased hepatic steatosis score (3.5 ± 0.6 vs. 2.7 ± 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-α or transforming growth factor-β 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.
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