[Metabolic aspects of alcoholic liver damage: 1984/5 update. 1. Epidemiology and alcohol metabolism].
In western industrialized countries ethanol is an important etiologic factor in the development of cirrhosis of the liver. Metabolic, immunologic and physico-chemical alterations of the hepatocyte due to ethanol are involved in the pathogenesis of alcoholic liver disease. However, the mechanisms by which ethanol damages the liver are far from clear. During the last two decades, the effect of ethanol on multiple biochemical pathways of the hepatocyte has been investigated intensively. The present paper is focusing on the metabolic aspects of alcoholic liver disease. In the first part of the review, special emphasis has been led on the metabolites of ethanol oxidation, while in the second part microsomal enzyme induction due to alcohol has been discussed. More than 90% of ethanol metabolism takes place in the liver via cytoplasmic alcoholdehydrogenase (ADH) and via a microsomal ethanol oxidizing system (MEOS). The products of these reactions are reduced nicotinadenine dinucleotide phosphate (NADH), acetaldehyde and acetate. NADH alters the redox state of the liver cell favouring all reductive processes. This shift in metabolic pathways results in hyperlactacidaemia, lactacidosis, ketosis and hyperuricaemia. Disturbances of the carbohydrate metabolism may lead either to hypo- or hyperglycaemia. The altered redox state also influences the metabolic pathways of lipid metabolism leading to lipid accumulation within the hepatocyte which can be morphologically observed as alcoholic fatty liver. In addition, porphyrin and collagen metabolism is also affected by the increased NADH/NAD+ ratio. On the other hand, acetaldehyde damages the microtubular system and the mitochondria. Acetaldehyde may also be responsible for the increased lipidperoxidation after chronic ethanol ingestion.
D000079:Acetaldehyde / Q000378:metabolism; D000138:Acidosis / Q000201:enzymology; D000426:Alcohol Dehydrogenase; D000428:Alcohol Drinking; D000429:Alcohol Oxidoreductases / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D003430:Cross-Sectional Studies; D005235:Fatty Liver, Alcoholic / Q000201:enzymology; D006801:Humans; D007662:Ketosis / Q000201:enzymology; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D008099:Liver / Q000201:enzymology; D008108:Liver Diseases, Alcoholic / Q000201:enzymology* / Q000453:epidemiology; D009243:NAD / Q000378:metabolism; D011166:Porphyrins / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D014527:Uric Acid / Q000097:blood
D007773:Lactates; D011166:Porphyrins; D011506:Proteins; D009243:NAD; D014527:Uric Acid; D019344:Lactic Acid; D003094:Collagen; D000429:Alcohol Oxidoreductases; D000426:Alcohol Dehydrogenase; D000079:Acetaldehyde
Metabolische Aspekte der alkoholischen Leberschädigung: Update 1984/85. Teil 1: Epidemiologie und Alkoholstoffwechsel.