[Alcohol induced changes of protein metabolism (author's transl].
An early manifestation of alcoholic liver injury is the accumulation of protein, as well as fat, in the liver. The increase in soluble proteins is associated with retention of water and swelling of the hepatocyte, resulting in hepatomegaly. Though "in vitro" ethanol inhibits hepatic protein synthesis, no consistent effects have been found after acute alcohol administration "in vivo". Moreover, after chronic alcohol consumption, the synthesis of liver protein is increased rather than decreased. Alcohol consumption, however, delays the secretion of proteins from the liver into the plasma, promoting accumulation in the liver of proteins which are primarily destined for export. The altered secretion is associated with decreased hepatic content of polymerized tubulin and visible disruption of microtubules, an organelle which may maintain the architectural organization required for transport of macromolecules. The alteration of microtubules has been linked to consequences of ethanol oxidation in the liver.
D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D000431:Ethanol / Q000009:adverse effects* / Q000378:metabolism; D006529:Hepatomegaly / Q000139:chemically induced; D006801:Humans; D008099:Liver / Q000187:drug effects; D008870:Microtubules / Q000187:drug effects; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D014404:Tubulin / Q000032:analysis
D011506:Proteins; D014404:Tubulin; D000431:Ethanol
Alkoholbedingt Störungen des Eiweissstoffwechsels.