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Urinary bile acid and bile alcohol excretion does not reflect the genetic polymorphism of debrisoquine hydroxylation.
Author(s) -
Karlaganis G,
Kupfer A,
Preisig R
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02374.x
Subject(s) - debrisoquine , hydroxylation , cholic acid , excretion , lithocholic acid , deoxycholic acid , chemistry , chenodeoxycholic acid , medicine , urine , alcohol , endocrinology , bile acid , biochemistry , pharmacogenetics , biology , genotype , gene , enzyme
Excretion of the major urinary bile alcohol 27‐nor‐5 beta‐cholestane‐3 alpha, 7 alpha, 12 alpha, 24,25‐ pentol, and of cholic, chenodeoxycholic, deoxycholic and lithocholic acid was measured in 24 h urine collections of 10 extensive and seven poor metabolizers of debrisoquine. There was no significant difference of the excretion of these cholesterol metabolites between the two groups, indicating that cholesterol hydroxylation to bile alcohols and bile acids is probably not controlled by the same genes responsible for the ‘debrisoquine‐ type’ hydroxylation polymorphism.