The peripheral metabolism of thyroid hormones and regulation of thyroidal status in poikilotherms

Abstract

Available data from poikilotherms (primarily salmonid teleosts and larval amphibians) indicate that, as in the intensively researched mammals, peripheral regulation of thyroidal status takes place. An extreme but physiologically plausible model is that the thyroidally secreted thyroxine (T4) is an inactive prohormone; the hypothalamic–hypophyseal–thyroidal axis may merely ensure that adequate T4 is secreted to serve as a substrate for conversion, by extrathyroidal 5′-monodeiodinase activity in various tissues, to the active thyroid hormone (TH), 3,5,3′-triiodo-L-thyronine (T3). Regulation of thyroidal status may be achieved at several peripheral levels by altering (i) TH transport from plasma into tissues, (ii) tissue T4 5′-monodeiodinase activity, and (iii) the capacities and possibly affinities of putative nuclear T3 receptor sites. Blind assumption in poikilotherms of the superficially similar mammalian model can be highly misleading since major differences exist between poikilotherms and mammals in (i) plasma protein – TH interactions, with secondary effects on plasma TH levels and kinetics, and (ii) pathways of T4 deiodination, possibly related to differences in iodide economy. In contrast, the nuclear TH receptor properties are phylogenetically conservative. However, the factors influencing their properties have been scarcely studied. In this regard variable body temperature, the distinguishing feature between poikilotherms and homeotherms, remains largely unexplored.