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Transcript
Alcohol Metabolism Relation to Liver Disease FAs NAD NADH + H+ Ethanol NAD Acetaldehyde Alcohol dehydrogenase NADH + H+ Acetyl CoA Acetaldehyde dehydrogenase TCA cycle NAD gets used up; decreased availability for glycolysis, Krebs, ETC B vitamin deficiency Pyruvate and acetyl CoA accumulate Acetyl CoA fatty acid synthesis FAs accumulate in the liver Once the liver is congested with fat: Decreased efficiency of hepatocytes Decreased conversion of vitamin D to active form Decreased gluconeogenesis Decreased glu & increased acetyl CoA ketosis (acidic) Accumulation of NADH + H+ (acidic) Excess NADH promotes pyruvate lactate (acidic) Interferes w/uric acid excretion (acid – gout symptoms) Decreased bile production Decreased oxygen distribution to liver cells Decreased immune function (decreased prot. synthesis as AAs are deaminated and C skeletons fat production) Can interfere w/drug metabolism Chronically: leads to fibrosis This cannot be corrected with diet; must abstain from alcohol use!