Study on NSAIDs and Test/Epitest Glucuronidation
- 12-06-2009, 06:00 PM
Study on NSAIDs and Test/Epitest Glucuronidation
Anyone care to interpret this study in the context of that age old debate of NSAIDs affecting protein synthesis? It is possible that this study has no relevance to that debate, but here it is anyway.
Steroids. 2009 Nov;74(12):971-7. Epub 2009 Jul 28.
Non-steroidal anti-inflammatory drugs interact with testosterone glucuronidation.
Sten T, Finel M, Ask B, Rane A, Ekström L.
Division of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Helsinki, FI-00014 Helsinki, Finland.
Testosterone and epitestosterone are secreted mainly as glucuronide metabolites and the urinary ratio of testosterone glucuronide to epitestosterone glucuronide, often called T/E, serves as a marker for possible anabolic steroids abuse by athletes. UDP-glucuronosyltransferase (UGT) 2B17 is the most important catalyst of testosterone glucuronidation. The T/E might be affected by drugs that interact with UGT2B17, or other enzymes that contribute to testosterone glucuronidation. Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used by sportsmen and we have examined the effect of two NSAIDs, diclofenac and ibuprofen, on testosterone and epitestosterone glucuronidation in human liver microsomes. In parallel, we have studied the inhibitory effect of these NSAIDs on recombinant UGT2B17 and UGT2B15, as well as other human hepatic UGTs that revealed low but detectable testosterone glucuronidation activity, namely UGT1A3, UGT1A4, UGT1A9 and UGT2B7. Both diclofenac and ibuprofen inhibited testosterone glucuronidation in microsomes, as well as UGT2B15 and UGT2B17. Interestingly, UGT2B15 was more sensitive than UGT2B17 to the two drugs, particularly to ibuprofen. Human liver microsomes lacking functional UGT2B17 exhibited significantly higher sensitivity to ibuprofen, suggesting that UGT2B15 plays a major role in the residual testosterone glucuronidation activity in UGT2B17-deficient individuals. Nonetheless, a minor contribution of other UGTs, particularly UGT1A9, to testosterone glucuronidation in such individuals cannot be ruled out at this stage. The epitestosterone glucuronidation activity of human liver microsomes was largely insensitive to ibuprofen and diclofenac. Taken together, the results highlight potential interactions between NSAIDs and androgen glucuronidation with possible implications for the validity of doping tests. - 12-06-2009, 08:07 PM
If NSAIDS inhibit glucuronidation, that means that taking NSAIDS actually slows down the bodies metabolism of testosterone. That's a good thing.
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- 12-07-2009, 12:24 PM
- 01-27-2010, 02:59 PM
It doesn't necessarily slow down the metabolism basically the study just says they interfere with the process. IDK if it slows it down or not it could just sayin.
basically NSAIDS could be used to skew an AAS screen test.
Your right but that's not what this study is about and that's not what the above poster was commenting on either. - 01-27-2010, 11:22 PM
^^What he said.
Often when people get mildly injured from say working out (it happens), they don't work out for a few weeks. So...does taking an NSAID to relieve pain and speed up recovery while you aren't even in the gym adversely affect protein synthesis (for instance)? My experience has led me to believe that it doesn't (for naproxen at least; haven't tried others). Unfortunately, there aren't many studies on this relatively common scenario. -
- 01-28-2010, 10:58 PM
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