The article discusses proposed physiological effects of reverse T3 (rT3), its synthesis and degradation. Until recently rT3 has been considered to be a metabolically inactive hormone present in high concentrations during the neonatal period and in various stress situations, including neoplasm development. Reverse T3 given to animals with unchanged hormonal homeostasis, especially of hormones participating in glucose and lipids metabolism seems to lack any metabolic effect. A fluctuation in circulating glucose and free fatty acids (FFA) levels is probably necessary for rT3 activity. In contrast to T3, rT3 acts hypo-metabolically by decreasing oxygen consumption, presumably as a result of reduced glucose and FFA utilization. A short latent period indicates that the action of rT3 is prevalently non-genomic. The article discusses the issue of low T3 syndrome or nonthyroidal syndrome which affects approximately 70% of hospitalized patients. The two hormones responsible for developing low T3 and high rT3 syndrome are: glucocorticoids . by inhibiting 5' deiodination and T3 synthesis followed by suppressed rT3 degradation, and adrenaline . by stimulating 5 deiodination followed by enhanced degradation of T3 and stimulated synthesis of rT3. Low T3 syndrome correlates with various cytokines. Cytokines treatment leads to the development of low Ta syndrome. In stress situations rT3 enhances the rise of glucose and FFA, whereas this rise is attenuated by rT3 when stress hormones i.e. glucocorticoids or catecholamine, are administered exogenously. We speculate that the molecular action of rT3 may be directed towards reducing T3 synthesis. It has been stated that equimolar concentrations of rT3 suppress 5.deiodination and synthesis of T3 with concomitant lower rT3 degradation. This leads to the development of T3 deficiency. T3 is a prohormone for synthesizing 3,5-diiodothyronine which, in turn, is necessary for binding and activating the cytochrom-c submit Va (Cyto-cVa) followed by increased oxidative phosphorylation and synthesis of ATP. Contrary to T3, rT3 decreases the ATP: ADP ratio. Finally, it is worth mentioning that the stimulatory-growth effect of rT3 on some tumor models in vitro was the most potent of all the various thyroid analogues. It may be suggested that lowered ATP reduces the energy supply of infected cells and thus suppresses the immune response.
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