Defective bile acid transport in an animal model of defective debrisoquine hydroxylation.
Bile acid transport in female DA (dark Aguti) rats, a model for debrisoquine hydroxylation deficiency in man, was investigated. Compared to hydroxylation competent male DA and Sprague-Dawley rats of either sex, the female DA rat had a significantly lower taurocholate maximal secretory rate in vivo. Studies in the perfused liver showed this to be due to a decreased extraction efficiency during exogenous taurocholate loading. To characterize further the defect, taurocholate uptake velocity into isolated hepatocytes was studied. This showed a decreased maximal uptake velocity in the female DA rat (P less than 0.02). Whether this defect in bile acid uptake is related to the defective debrisoquine hydroxylation, remains to be established.
D000818:Animals; D001646:Bile / Q000378:metabolism; D001647:Bile Acids and Salts / Q000378:metabolism*; D001692:Biological Transport; D003647:Debrisoquin / Q000378:metabolism*; D005260:Female; D006900:Hydroxylation; D007546:Isoquinolines / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains / Q000378:metabolism*; D013656:Taurocholic Acid / Q000378:metabolism
D001647:Bile Acids and Salts; D007546:Isoquinolines; D013656:Taurocholic Acid; D003647:Debrisoquin