Recently reported that 3-T1AM metabolism produces inactive 3-iodothyroacetic acid. In this way, we demonstrated that 3-T1AM's rapid cardiac and thermogenic effects depend on the ethylamine side chain. No iodinated T0AM is produced when 3-T1AM is used as a substrate by Dio1 and Dio3 enzymes, as evidenced by in vitro data. As a result, we were curious about the possibility that deiodination might also function as an inactivation mechanism for 3-T1AM. Due to the fact that T0AM did not cause bradycardia or anapyrexia in mice upon single or repeated administration, our in vivo experiments demonstrate that it does not possess the metabolic, cardiovascular, or thermoregulatory properties of 3-T1AM. Additionally, T0AM did not affect TH homeostasis because it did not affect TH-regulated genes or serum or liver TH concentrations. Previous research has demonstrated that T3 regulates hepatic trace element metabolism (such as Se). By administering T0AM and 3-T1AM, we set out to see if these effects might be at least partially mediated by TAMs. According to our investigations, the major trace element storage, metabolism and transport proteins as well as Se status in serum, liver and kidneys were unaffected by T0AM's repeated administration. Therefore, in our paradigm, T0AM exhibits very little biological activity in comparison to reports of 3-T1AM, which is physiologically more active.
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Reports in Thyroid Research received 2 citations as per Google Scholar report
