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Old 06-13-2004, 02:57 AM
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Join Date: Jun 2004
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question/explanation alcohol

A 49-year-old male presents with symptoms that developed following a long weekend of binge drinking. His serum reveals a -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 which of the following?


Choices
A. Decreased free fatty acid delivery to the liver
B. Decreased production of triglycerides
C. Increased mitochondrial oxidation of fatty acids
D. Increased NADH production
E. Increased release of lipoproteins



Answer : D
Explanation
Alcohol can produce hepatic steatosis via several mechanisms, such as increased fatty acid synthesis, decreased triglyceride utilization, decreased fatty acid oxidation, decreased lipoprotein excretion, and increased lipolysis. Ethanol is taken up by the liver and is converted into acetaldehyde by either alcohol dehydrogenase (the major pathway), microsomal P-450 oxidase, or peroxisomal catalase. These pathways also convert 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.
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