1. This study investigated the glucuronidation of propranolol and its equipotent phase 1 metabolite 4-hydroxypropranolol by all 19 members of the human UGT1 and UGT2 families.
2. UGT1A7, UGT1A9, UGT1A10 and UGT2A1 were found to glucuronidate propranolol, with different stereoselectivity for each enzyme.
3. Modeling and molecular docking studies were performed to explain the stereoselective glucuronidation of the substrates under study.
The article is generally reliable and trustworthy in its reporting of the research conducted on the glucuronidation of propranolol and its equipotent phase 1 metabolite 4-hydroxypropranolol by all 19 members of the human UGT1 and UGT2 families. The authors provide a detailed description of their methodology, results, and conclusions, as well as a thorough discussion of their findings. The article does not appear to be biased or one-sided in its reporting; rather, it presents both sides equally by providing evidence for both positive and negative results from their experiments. Furthermore, potential risks are noted throughout the article, such as possible adverse effects from taking propranolol or other drugs that may be affected by glucuronidation.
The only potential issue with this article is that it does not explore any counterarguments or alternative explanations for their findings. While this is understandable given the scope of this particular study, it would have been beneficial to include some discussion on other possible explanations for their results or any unexplored areas that could be further investigated in future studies. Additionally, there is no promotional content present in this article; rather, it provides an objective overview of the research conducted without any bias towards any particular outcome or conclusion.