The enlargements of liver size induced by orotic acid and di (2-ethyl hexyl) phthalate occur in different metabolic pathways.

ABSTRACT

The present study was conducted to elucidate the metabolic pathways by which enlarged liver size of patients undergoing disorders of orotic acid de novo metabolism and those patients of enlarged liver size induced by di(2-ethyl hexyl) phthalate in rats as animal model. The results showed that rats-treated with orotic acid generated liver triglyceride content 400% higher than that of the control accompanied with a significant decrease of phospholipid levels (P<0.05). The rates of lipogenic enzymes, both fatty acid synthase (FAS) and phosphatidate phosphohydrolase (PAP), increase accompanying promotions of liver triglyceride content without any changes in fatty acid degradation pathway. However, those rats-treated with di(2- ethyl hexyl) phthalate generated liver phospholipid level significantly higher than of the control accompanied with a markedly decreased the liver triglyceride levels. Both FAS and PAP activities were almost similar with those controls but the rates of fatty acid degradation were increased approximately by 2.5-fold of control. In conclusion: The enlargement of liver size induced by orotic acid is associated with largely retains triglyceride molecules in liver tissues, whereas those induced by di(2-ethyl hexyl) is associated with the induction of phosphorylation generating an increase of liver phospholipid levels.