The metabolism of ethanol by the liver increases the NADH/NAD+ ratio reducing its ability to perform gluconeogenesis.
Ethanol is oxidised to acetaldehyde in the liver cytoplasm by alcohol dehydrogenase. This is oxidised to acetate by acetaldehyde dehydrogenase in the mitochondria. Two NADH molecules are produced in the liver cell from each ethanol molecule. Intake of large amounts of alcohol results in the cellular NADH/NAD+ ratio being increased. Several dehydrogenases such as lactate dehydrogenase can be inhibited by this so that the pyruvate/lactate equilibrium is disturbed resulting in reduced amounts of pyruvate available for gluconeogenesis. Excessive drinking often results in reduced food intake so that dietary sources of glucose diminish. This coupled with impaired gluconeogenesis can result in inadequate supply of glucose to the brain in extreme cases with dangerous consequences.*##**##*
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