In conclusion, we characterized the thyroxine glucuronidation in human liver, intestine, and kidney microsomes and found that UGT1A1 in the
liver, UGT1A8
and UGT1A10 in the intestine,
and UGT1A7, UGT1A9,
and UGT1A10 in the kidney mainly contribute to the activity. The change of activities of these UGTs via inhibition and induction by administered drugs (Kiang et al., 2005) as well as genetic polymorphisms (Miners et al.