Fatty change (steatosis) of the liver in alcoholism is reversible. The predominant mechanism of lipid accumulation in hepatocytes with chronic alcohol use is:
- A Increased hepatic lipolysis mobilizing free fatty acids from adipose
- B Excess NADH from alcohol oxidation inhibiting fatty acid beta-oxidation and promoting triglyceride synthesis ✓
- C Upregulation of VLDL secretion overwhelming export capacity
- D Direct toxicity of acetaldehyde causing peroxisomal dysfunction
Correct answer: B. Excess NADH from alcohol oxidation inhibiting fatty acid beta-oxidation and promoting triglyceride synthesis
Explanation
Ethanol oxidation by alcohol dehydrogenase and ALDH generates large amounts of NADH, shifting the NAD+/NADH ratio. High NADH inhibits fatty acid beta-oxidation (which requires NAD+), diverts pyruvate to lactate, and promotes fatty acid synthesis. This combination—reduced oxidation and increased synthesis—leads to triglyceride accumulation in hepatocytes. VLDL secretion is actually impaired (not upregulated) in alcoholic liver disease.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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