Pathogenesis of alcoholic hepatic steatosis

Abstract

Chronic alcohol misuse is the most common cause of hepatic steatosis. The accumulation of lipid is reversible with abstinence, but some workers have suggested that the severity of hepatic steatosis predicts the progression with time to alcoholic cirrhosis. Triacylglycerol is the major accumulating lipid and subcellular fractionation and electron microscopy studies have shown accumulation of lipid droplets within the golgi fraction. This is consistent with the reports in both experimental animals and man of reduced hepatic secretion of very low density lipoprotein triacylglycerol which may be secondary to acetaldehyde-induced disruption of the cytoskeletal elements. In addition, hepatic production of triacylglycerol increases, but most studies in animal models suggest that increased triacylglycerol synthesis becomes less important as hepatic lipid accumulates.

Depression by a Green Tea Extract of Alcohol-Induced Oxidative Stress and Lipogenesis in Rat Liver

“…34,46) The results of this present study provide consistent evidenced that 30 d of 36% alcohol gavage increased the liver and bile ROS levels, Kupffer cell infiltration, 4-HNE staining, and CYP2E1 and NADPH oxidase p47phox protein expression, subsequently con- tributing to alcoholic liver disease. The progression of alcoholic liver disease involves the early appearance of alcoholic steatosis 1,4) and subsequent alcoholic hepatitis and cirrhosis. 2,4) Ethanolinduced hepatosteatosis could be caused by the inhibition of fatty acid oxidation and the enhancement of lipogenesis.…”

“…The progression of alcoholic liver disease involves the early appearance of alcoholic steatosis 1,4) and subsequent alcoholic hepatitis and cirrhosis. 2,4) Ethanolinduced hepatosteatosis could be caused by the inhibition of fatty acid oxidation and the enhancement of lipogenesis. An increased triglyceride content in alcohol-treated hepatocytes has resulted from the inhibition of fatty acid oxidation.…”

“…[4][5][6] Previous studies have implicated that catechins 24,25,31,33) or caffeine 33) supplementation reduced inflammation, oxidative stress and lipogenesis in the alcoholic liver. We therefore investigated that notion that adding a green tea extract containing catechins and caffeine to alcohol could effectively reduce chronic alcohol-induced oxidative stress, inflammation and lipogenesis in the liver.…”

“…[1][2][3][4] Alcoholic fatty liver is the early pathological stage of alcoholic liver diseases which are regulated by sterol regulatory element-binding proteins (SREBP) containing SREBP1a, SREBP-1c and SREBP-2. [4][5][6] SREBP-1c regulated fatty acid synthesis, whereas SREBP-2 regulated cholesterol synthesis in the liver. 6) Overexpression of SREBP-1a and SREBP-1c increased the cholesteryl esters, triglyceride accumulation and fatty acid synthesis in transgenic mice leading to fatty liver.…”

A Critical Evaluation of Hepatic Resection in Cirrhosis: Optimizing Patient Selection and Outcomes

“…Steatosis of the donor liver has been widely studied as an adverse prognostic marker in liver transplantation [53, 54]. The etiologies of hepatic steatosis are multiple, and it is associated with a variety of states such as alcohol injury, obesity, postischemic states, or other toxins including certain chemomerapeutics [55, 56, 57]. Though prediction is unreliable, steatosis is generally present when the liver is subjected to oxidative stress [56], presumably increasing the risk of hepatectomy.…”