Ethanol and protein turnover

Protein turnover can be profoundly influenced by ethanol intake in humans. The effects of ethanol are mostly due to its oxidation and oxidative by-products, are dose related and dependent upon the drinking pattern. Acute alcohol drinking in non-habitual ethanol users induces a shift in liver redox state that appears to be responsible for a reduction in liver export protein synthesis and/or secretion. The production of reducing equivalents combined with increased acetate availability in the peripheral tissues are likely to be responsible for the reduced protein oxidation rate observed in these circumstances. Chronic ethanol abuse induces loss of nitrogen and muscle wasting with different mechanisms. Despite several discrepancies between studies performed to assess the mechanisms of protein loss in chronic ethanol abuse, it is reasonable to hypothesize that tissue-specific imbalances between protein synthesis and protein catabolism are probably responsible for the loss of nitrogen in habitual alcohol abusers. A number of studies have shown that skeletal muscle protein synthesis is reduced with chronic alcohol abuse, whereas indirect evidence suggests that increased intestinal protein breakdown might be responsible for the reduction in intestinal protein content. In conclusion, there is the need for new studies focusing on the effects of ethanol on the turnover rate of specific tissues and proteins. Given the recent evidence of a protective effect of moderate alcohol intake on the cardiovascular system, particular attention should be paid to dose-response studies in habitual drinkers of low to moderate doses of alcohol.