Cholestyramine treatment reduces postprandial but not fasting serum bile acid levels in humans.
Fasting serum concentrations of cholic acid, chenodeoxycholic acid, and deoxycholic acid were determined in healthy subjects and in patients with familial hypercholesterolemia before and during treatment with cholestyramine. The bile acids were analyzed by a specific isotope-dilution technique by using gas chromatography-mass spectrometry. Cholestyramine treatment did not change the fasting concentration of total bile acids, but the contribution of cholic acid was increased; those of chenodeoxycholic acid and deoxycholic acid were decreased. No decrease of fasting bile-acid concentrations in portal venous serum was seen in 2 cholestyramine-treated gallstone patients. The postprandial total bile-acid concentration was about 40% lower during cholestyramine treatment in healthy subjects, reflecting a reduced postprandial inflow of bile acids to the liver. This degree of interruption of the postprandial enterohepatic circulation may be sufficient to produce a near maximal bile-acid biosynthesis rate and to promote lowering of plasma cholesterol also in the fasting state. It is concluded that the postprandial bile-acid inflow to the liver may be more important as a regulator of bile-acid biosynthesis than is the fasting level of bile acids.
D001647:Bile Acids and Salts / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL; D002792:Cholestyramine Resin / Q000627:therapeutic use*; D004435:Eating; D005215:Fasting; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000188:drug therapy; D008077:Lipoproteins, LDL / Q000097:blood; D008102:Liver Circulation
D001647:Bile Acids and Salts; D008078:Cholesterol, LDL; D008077:Lipoproteins, LDL; D002792:Cholestyramine Resin; D002784:Cholesterol