A chronic alcoholic has hepatomegaly with large clear vacuoles displacing hepatocyte nuclei. Which mechanism best explains hepatic triglyceride accumulation in this setting?
- A Impaired synthesis of apolipoprotein B required for triglyceride export from hepatocytes ✓
- B Increased catabolism of stored lipid releasing free fatty acids into hepatocytes
- C Deficiency of lysosomal acid lipase causing intracellular lipid storage
- D Accumulation of undegraded cholesterol esters in lysosomes
Correct answer: A. Impaired synthesis of apolipoprotein B required for triglyceride export from hepatocytes
Explanation
Alcohol increases NADH generation, favoring fatty acid synthesis, but a key mechanism of steatosis is impaired assembly and secretion of very low density lipoproteins because of defective apolipoprotein synthesis, trapping triglyceride within hepatocytes. The same mechanism explains fatty change in CCl4 poisoning and protein malnutrition. Lysosomal acid lipase deficiency causes cholesterol ester storage disease, and lysosomal cholesterol ester accumulation describes Niemann-Pick disease type C, both distinct entities.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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