| Literature DB >> 8964844 |
J M Koopdonk-Kool1, J J de Vijlder, G J Veenboer, C Ris-Stalpers, J H Kok, T Vulsma, K Boer, T J Visser.
Abstract
Thyroid hormones are essential for fetal development. T4 can be activated by type I (ID-I) and type II (ID-II) iodothyronine deiodinase or inactivated by type III deiodinase (ID-III). The influence of placental ID-II and ID-III on the regulation of fetal thyroid hormone levels was investigated. Using [125I]T4 and [125I]T3, respectively, ID-II and ID-III activities were measured in homogenates of normal human placentas from 6-43 weeks gestational age and in placentas from five term neonates with a total thyroid hormone synthesis defect. ID-II and ID-III activities related to protein or DNA concentration decreased and total placental ID-III activity increased significantly during pregnancy, whereas the increase in total placental ID-II activity was not significant. Absolute placental ID-II activity was approximately 200 times lower than ID-III activity at all gestational ages. Therefore, fluctuations in ID-II activity were not likely to have a significant influence on fetal thyroid hormone concentrations, but may play a role in the regulation of intraplacental T3 generation. The high ID-III activity most likely influences the thyroid hormone economy of the fetus. Severely hypothyroid newborns showed strongly decreased serum T4 levels, but serum T3 and placental ID-III activities were similar to those in euthyroid newborns. These results suggest that placental ID-III activity is regulated by serum T3, but not by serum T4.Entities:
Mesh:
Substances:
Year: 1996 PMID: 8964844 DOI: 10.1210/jcem.81.6.8964844
Source DB: PubMed Journal: J Clin Endocrinol Metab ISSN: 0021-972X Impact factor: 5.958