A 49-year-old male presents with symptoms that developed following a long weekend of binge drinking. His serum reveals a g-glutamyl transferase (GGT) level of 65 IU/L. A liver biopsy reveals fatty change (steatosis) of numerous hepatocytes. This patient's liver abnormality is most likely the result of
Alcohol can produce hepatic steatosis several mechanisms, such as increased fatty acid synthesis, decreased triglyceride utilization, decreased atty acid oxidation, decreased lipoprotein excretion, and increased lipolysis. Ethanol is taken up by the liver and is conveed into acetaldehyde by either alcohol dehydrogenase (the major pathway), microsomal P-450 oxidase, or peroxisomal catalase. These pathways also conve nicotinamide adenine dinucleotide (NAD) to NADH. This excess production of NADH changes the normal hepatic metabolism away from catabolism of fats and toward anabolism of fats (lipid synthesis), resulting in decreased mitochondrial oxidation of fatty acids and increased hepatic production of triglyceride. Ethanol also increases lipolysis and inhibits the release of lipoproteins. Increased lipolysis increases the amount of free fatty acids that reach the liver. Reference: Robbins & Cotran Pathologic Basis of Disease, 9edition
Decreased free fatty acid delivery to the liver
Decreased production of triglycerides
Increased mitochondrial oxidation of fatty acids
Increased NADH production
miscellaneous