Letter to Editor Deiodinases and Developmental Hypothyroidism (original) (raw)

Thyroid hormones (THs) are crucial for normal organ development [1-30]. The levels of 3,5,3'-triiodothyronine (T3) in tissues is regulated by the action of the iodothyronine deiodinases (DI, DII, and DIII) [4,31-33]. In 2015b, I reported that any defects in fetal Ds may have more impact on fetal brain since they can result in intracellular T3 deficiency despite sufficient maternal TH supply. Also, my group [24] reported that hypothyroidism during the critical developmental period caused elevation in D2 activity in the diencephalon and mesen-cephalon, revealing of a compensatory response. This reflects that the compensatory action of Ds to changed TH level is not yet mature in young embryos or fetuses [32-34]. However, MMI treatment did not meaningfully change the activities of D1or D3 in maternal liver and kidney. Thus, further studies are needed to elucidate the tissue-, cell-, and sex-specific expression of individual Ds during the development of both human and animals, in the adult, during aging and when sick.