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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





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
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!