Comparative aspects of maturation and control of thyroid-hormone deiodination during development

• Main Authors: Darras, Veerle, Kühn, Eduard, Decuypere, Eddy
• Format: Article in Journal/Newspaper
• Language: English
• Published: Laser pages publ ltd 1994
• Subjects: i iodothyronine deiodinase; rana-catesbeiana tadpoles; thyroxine 5'-monodeiodinase activity; hepatic 5'-deiodinase activity; parr-smolt transformation; salmon salmo-salar; low body-weight; growth-hormone; rainbow-trout; oncorhynchus-mykiss; Salmo salar
• Online Access: https://lirias.kuleuven.be/handle/123456789/61638; https://lirias.kuleuven.be/bitstream/123456789/61638/1//Darras+et+al._1994_Israel+Journal+of+Zoology_vol40-p383-400.pdf

In all vertebrates the main secretory product of the thyroid gland is thyroxine (T-4). The rate of its conversion to the active triiodothyronine (T-3) or to the inactive reverse T-3 (rT(3)) can be regulated in the peripheral tissues by deiodination. Probably all vertebrates are capable of both outer and inner ring deiodination (ORD and IRD), catalyzed by deiodinases. Most of these enzymes are related to one of the three mammalian deiodinase types, but the abundance and tissue localization can differ substantially among vertebrate groups. During ontogeny high plasma levels of T-3 occur around the period of birth in mammals, of hatching in birds, and of metamorphosis in amphibians. This T-3 increase seems to be not only the result of increased T-3 production (ORD), but also in considerable degree of decreased T-3 degradation (IRD). In fish, birds, and mammals growth hormone can increase plasma T-3 levels. In chickens this effect is obtained not by increasing the amount of active hepatic T-3-producing (type I) enzyme, but by inactivation or degradation of hepatic T-3-degrading (type III) enzyme. status: published