Abstract
Summary
The administration of a single dose of D-galactosamine (1.5 g/kg) results in hepatocellular necrosis and fatty liver in the rat. Hepatic triglyceride accumulation is not altered by administration of adenine, ATP, uridine, uridine nucleotides, or uridine di-phosphoglucose.
Protein synthesis in vivo is impaired as early as 4 hr after administration of D-galactosamine. Subsequently the expected post-Triton WR 1339 hypertriglyceridemia is reduced and beta-lipoproteins are decreased by electrophoretic analysis. These data suggest that impaired hepatic lipoprotein release, presumably due to inhibition of synthesis of the protein moiety of lipoprotein, is the mechanism of the D-galactosamine-induced fatty liver.
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