Disease relevance of Fatty Liver, Alcoholic

• The present findings suggest a novel paradigm for dietary fatty acids in the pathogenesis of alcoholic liver disease and provide a promising therapeutic strategy-nutritional modulation of adiponectin-in treating human alcoholic fatty liver disease [1].
• In the three groups of patients with minimal, potentially reversible liver disease (31 patients with alcoholic fatty liver, 10 with viral hepatitis, and 18 with biliary disease) plasma concentrations of proline and the three branched chain amino-acids were significantly reduced [2].
• The disposition profile of ceftriaxone was studied in eight normal subjects and in 15 subjects with various degrees of chronic liver damage (alcoholic fatty liver [FL] and cirrhosis without [C] and with [CA] ascites) who received bolus injections of ceftriaxone, 1 gm iv [3].
• Levels of IL-8 in patients with alcoholic fatty liver, alcoholic cirrhosis and viral hepatitis were higher than those in controls and in patients with non-alcoholic fatty liver [4].
• The mean serum retinol level in patients with alcoholic cirrhosis was 0.68 +/- 0.38 mumol/l compared with 1.99 +/- 1.14 mumol/l in patients with alcoholic fatty liver (P less than 0.03) [5].

High impact information on Fatty Liver, Alcoholic

• Rats fed ethanol-containing diets for 37 days showed remarkable increase in hepatic lipids and lipid droplet accumulation in the hepatocytes, indicating the onset of alcoholic fatty liver [6].
• CONCLUSIONS: Taken together, our findings suggest that AMPK may play a key role in regulating the effects of ethanol on SREBP-1 activation, fatty acid metabolism, and development of alcoholic fatty liver [7].
• This study aimed to examine if pioglitazone, an antidiabetic reagent serving as a ligand of peroxisome proliferator-activated receptor gamma (PPAR gamma), could prevent alcoholic fatty liver [8].
• Adiponectin and alcoholic fatty liver: Is it, after all, about what you eat [9]?
• In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha improves AFLD [10].

Chemical compound and disease context of Fatty Liver, Alcoholic

• Increased esterification of fatty acids to triglyceride is common to most of the mechanisms proposed to explain the causation of alcoholic fatty liver [11].
• The activity of the metabolic form of hepatic phosphatidate phosphohydrolase correlates with the severity of alcoholic fatty liver in human beings [11].
• The activities of other enzymes such as aspartate aminotransferase, alanine aminotransferase and glutamate dehydrogenase remained virtually unchanged in the liver of patients with alcoholic fatty liver but were strikingly enhanced in the serum [12].
• Patients with alcoholic fatty liver also showed significantly reduced plasma phenylalanine values [2].
• Treatment of alcoholic fatty liver: is the metabolic effect of metadoxine the only reason for improved liver function [13]?

Biological context of Fatty Liver, Alcoholic

• Thus, the data suggest that: 1) the increased plasma mAspAT observed in alcoholics may reflect pharmacologic upregulation of mAspAT mRNA and of mAspAT synthesis by ethanol; and 2) increased mAspAT-mediated fatty acid uptake may contribute to alcoholic fatty liver [14].
• These results suggest that depressed lipolysis due to a relative deficiency of triglyceride lipase is not a causal factor in triglyceride accumulation in chronic alcoholic fatty liver [15].
• The protective action of the anti-oxidants suggests that lipid peroxidation (probably initiated by acetaldehyde) is an important event in the pathogenesis of acute alcoholic fatty liver [16].

Anatomical context of Fatty Liver, Alcoholic

• Mitochondria were isolated from needle liver biopsies from normal subjects, from patients with alcoholic fatty liver and patients with fatty liver of other aetiologies, incubated with 60 mumol/l [U-14C]hexadecanoate and the resultant CoA and carnitine esters were measured [17].
• In the rat, the liquid diet technique provides a model for the alcoholic fatty liver, various alcohol-induced metabolic, endocrine and central nervous system abnormalities (including tolerance and dependence) and the interaction of ethanol with industrial solvents, many commonly used drugs, analgesics, carcinogens and nutrients [18].
• Effect of ursodeoxycholic acid on prostaglandin metabolism and microsomal membranes in alcoholic fatty liver [19].

Gene context of Fatty Liver, Alcoholic

• Impairment of PPARalpha function during ethanol consumption contributes to the development of alcoholic fatty liver, which can be overcome by Wy14,643 [20].
• In conclusion, the protective action of saturated fat against the development of alcoholic fatty liver in mice is partially mediated through induction of adiponectin [1].
• No significant differences of TGF-beta 1 mRNA expression were observed between alcoholic fatty liver men and alcohol abusers [21].
• Our results have indicated that alcoholic fatty liver may differentially induce CINC-1 production and hepatic necrosis after I/R [22].
• Hepatic gamma-glutamyltransferase activity in alcoholic fatty liver: comparison with other liver enzymes in man and rats [12].

Analytical, diagnostic and therapeutic context of Fatty Liver, Alcoholic

• CONCLUSIONS: In patients with alcoholic fatty liver, metadoxine accelerates the normalization of liver function tests and the ultrasonographic changes, even in those who do not completely abstain from alcohol intake [23].
• Oral administration of S-nitroso-N-acetylcysteine prevents the onset of non alcoholic fatty liver disease in rats [24].
• Higher concentrations of IL-6 may be required to protect against alcoholic fatty liver isograft injury because alcohol inhibits IL-6 signaling in the liver [25].

References