Abstract
Interference with the enterohepatic circulation leads to changes in plasma lipoprotein metaholism. Thus, increased bile acid synthesis (such as after cholestyramine therapy or biliary diversion) stimulates hepatic triglyceride production and increases the number of low density lipoprotein (LDL) receptors in the liver. However, treatment with chenodeoxycholic acid reduces triglyceride production and appears to reduce LDL catabolism. Ursodeoxycholic acid therapy, which has minor effects on bile acid synthesis, results in relatively minor changes in lipoprotein metabolism. A tendency for lowered LDL cholesterol levels may be related to the fact that ursodeoxycholic acid interferes with the enterohepatic circulation of the normal bile acids, particularly when administered at a high dosage.
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