Abstract
Thyroxine (T4) is the major thyroid hormone in the thyroid gland and the circulation. However, it is widely accepted on the basis of abundant evidence that 3,5,3'-triiodothyronine (T3) is responsible for most, if not all, of the physiological effects of TH in extrathyroidal tissues, and T4 functions as the pro-hormone. Whether T4 has any intrinsic activity per se or is merely a pro-hormone that must be converted to T3 in order to exert any TH action has yet to be resolved. Although there are some physiological actions of T4 that are mediated by receptors at the cell membrane (non-genomic effects), the vast majority of the physiological effects of the THs identified to date involve the binding of T3 to specific nuclear receptors to regulate gene expression (genomic effects). This review examines how the role of T4 in genomic TH action has been viewed and debated during the hundred years since it was first isolated in 1914.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
