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The mechanism(s) of the alcohol-induced impairment in glycogen synthesis in oxidative skeletal muscles.

Ethanol is known to acutely inhibit glucose-stimulated glycogen deposition in skeletal muscles in the rat. This effect is selective for oxidative as opposed to non-oxidative muscles. This paper explores the biochemical basis for this selective impairment in muscle glycogen metabolism. 4-Methylpyrazole, a potent inhibitor of alcohol dehydrogenase, potentiated the ethanol-mediated impairment in glycogen deposition in oxidative muscles and was associated with abnormalities in glycogen deposition in non-oxidative muscles. By contrast, disulfiram, a potent inhibitor of aldehyde dehydrogenase had no effect on the ethanol-mediated impairment in glycogen deposition in both oxidative and non-oxidative muscles. The implication is that it is the ethanol molecule itself, and not one of its metabolites (acetaldehyde, acetate, excess NADH), that mediates the defect in glycogen metabolism.