A model of in vitro UDP-glucuronosyltransferase inhibition by bile acids predicts possible metabolic disorders

J Lipid Res. 2013 Dec;54(12):3334-44. doi: 10.1194/jlr.M040519. Epub 2013 Oct 10.

Abstract

Increased levels of bile acids (BAs) due to the various hepatic diseases could interfere with the metabolism of xenobiotics, such as drugs, and endobiotics including steroid hormones. UDP-glucuronosyltransferases (UGTs) are involved in the conjugation and elimination of many xenobiotics and endogenous compounds. The present study sought to investigate the potential for inhibition of UGT enzymes by BAs. The results showed that taurolithocholic acid (TLCA) exhibited the strongest inhibition toward UGTs, followed by lithocholic acid. Structure-UGT inhibition relationships of BAs were examined and in vitro-in vivo extrapolation performed by using in vitro inhibition kinetic parameters (Ki) in combination with calculated in vivo levels of TLCA. Substitution of a hydrogen with a hydroxyl group in the R1, R3, R4, R5 sites of BAs significantly weakens their inhibition ability toward most UGTs. The in vivo inhibition by TLCA toward UGT forms was determined with following orders of potency: UGT1A4 > UGT2B7 > UGT1A3 > UGT1A1 ∼ UGT1A7 ∼ UGT1A10 ∼ UGT2B15. In conclusion, these studies suggest that disrupted homeostasis of BAs, notably taurolithocholic acid, found in various diseases such as cholestasis, could lead to altered metabolism of xenobiotics and endobiotics through inhibition of UGT enzymes.

Keywords: cholestasis; endobiotics; structure-UDP-glucuronosyltransferase inhibition relationship; xenobiotics.

Publication types

  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biocatalysis / drug effects
  • Enzyme Inhibitors / pharmacology*
  • Glucuronosyltransferase / antagonists & inhibitors*
  • Glucuronosyltransferase / chemistry
  • Glucuronosyltransferase / metabolism*
  • Humans
  • Hymecromone / metabolism
  • Intestines / enzymology
  • Kinetics
  • Liver / enzymology
  • Metabolic Diseases / enzymology*
  • Models, Molecular
  • Protein Conformation
  • Taurolithocholic Acid / pharmacology*
  • Trifluoperazine / metabolism

Substances

  • Enzyme Inhibitors
  • Trifluoperazine
  • Hymecromone
  • Taurolithocholic Acid
  • Glucuronosyltransferase