Document Detail

Role of thyroid hormone during early brain development.
MedLine Citation:
PMID:  15554884     Owner:  NLM     Status:  MEDLINE    
The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia - defined as thyroxine (T4) concentrations that are low for the stage of pregnancy - is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain. Despite a highly efficient uterine-placental 'barrier' to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the 'free' T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and 'free' T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy. The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor. Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.
Gabriella Morreale de Escobar; María Jesús Obregon; Francisco Escobar del Rey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  European journal of endocrinology / European Federation of Endocrine Societies     Volume:  151 Suppl 3     ISSN:  0804-4643     ISO Abbreviation:  Eur. J. Endocrinol.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-23     Completed Date:  2005-01-05     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  9423848     Medline TA:  Eur J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  U25-37     Citation Subset:  IM    
Instituto de Investigaciones Biomedicas Alberto Sols, Consejo Superior de Investigaciones Cientificas (CSIC) y Universidad Autonoma de Madrid (UAM), Arturo Duperier, 4, 28029-Madrid, Spain.
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MeSH Terms
Brain / embryology*,  metabolism
Hypothyroidism / complications
Iodine / deficiency
Maternal-Fetal Exchange*
Pregnancy Complications
Pregnancy Trimester, First
Receptors, Thyroid Hormone / metabolism
Thyroid Hormones / physiology*
Reg. No./Substance:
0/Receptors, Thyroid Hormone; 0/Thyroid Hormones; 7553-56-2/Iodine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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