Type 1 iodothyronine deiodinase in human physiology and disease

摘要: Thyroid hormone is essential for the normal function of virtually all tissues. The iodothyronine deiodinases catalyze removal an iodine residue from pro-hormone thyroxine (T4) molecule, thus producing either active form triiodothyronine (T3; activation) or inactive metabolites (reverse T3; inactivation). Type I deiodinase (D1) catalyzes both reactions. Over last years, several studies have attempted to understand mechanisms D1 function, underlying its effects on thyroid metabolism and pathological processes. Although peripheral D1-generated T3 production contributes a portion plasma in euthyroid state, pathologically increased thyroidal activity seems be main cause elevated concentrations observed hyperthyroid patients. On other hand, D1-deficient mouse models show that, absence D1, lesser iodothyronines are excreted feces with loss associated iodine, demonstrating scavenging that might particularly important deficiency setting. Polymorphisms DIO1 gene been changes serum levels, whereas decreased has reported nonthyroid illness syndrome human neoplasias. current review aims at presenting updated picture recent advances made biochemical molecular properties as well role physiology.