Early expression of thyroid hormone deiodinases and receptors in human fetal cerebral cortex

Chan, Shiao-Yng; Kachilele, Stivelia; McCabe, Chris; Tannahill, Lesley; Boelaert, Kristien; Gittoes, Neil; Visser, Theo J.; Franklyn, Jayne A.; Kilby, Mark

doi:10.1016/s0165-3806(02)00459-5

Cited by 93 publications

(61 citation statements)

References 35 publications

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“…Evidence from a range of scientific disciplines suggests that perinatal and obstetric factors are determinants of offspring mental health in later life stages (1,13,41,42,43,44,45,46,47). In this review, which focused on behavioural and psychiatric disorders of offspring born from mothers with thyroid dysfunction during pregnancy, we found that maternal thyroid dysfunction was associated with offspring mental health problems not only in early childhood but also in late adolescence and adulthood.…”

Section: Discussionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Maternal thyroid dysfunction during pregnancy and behavioural and psychiatric disorders of children: a systematic review

Fetene

Betts

Alati

2017

European Journal of Endocrinology

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Background: Maternal thyroid dysfunction during pregnancy may lead to persistent neurodevelopmental disorders in the offspring appearing in later life. This study aimed to review the available evidence concerning the relationship between maternal thyroid status during pregnancy and offspring behavioural and psychiatric disorders. Methods: Systematic electronic database searches were conducted using PubMed, Embase, PsycNET, Scopus, Google Scholar and Cochrane library. Studies including gestational thyroid dysfunction as the exposure and offspring behavioural and psychiatric disorders as the outcome were included. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed and, after thorough screening by two independent reviewers, 13 articles remained eligible for inclusion in this study. Results: Indicators of maternal thyroid dysfunction, including low and high thyroid hormone level and autoimmune thyroiditis, during early pregnancy, were found to be associated with several offspring behavioural and psychiatric disorders such as attention deficit hyperactivity disorder (ADHD), autism, pervasive developmental problems, externalising behaviour, in addition to epilepsy and seizure. The majority of associations were found with low maternal thyroid hormone level. Conclusion: Maternal thyroid function during pregnancy, particularly hypothyroidism, is associated with behavioural and psychiatric disorders in children. Further studies are needed with a capacity to adjust for a fuller range of confounding factors.

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Section: Discussionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Maternal thyroid dysfunction during pregnancy and behavioural and psychiatric disorders of children: a systematic review

Fetene

Betts

Alati

2017

European Journal of Endocrinology

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“…The various TRa (THRA) and TRb (THRB) isoforms are expressed in the fetus in a tissuespecific manner by mid-gestation and often at gestational ages earlier than the appearance of thyroid hormones in the fetal circulation (Table 1; Bernal & Pekonen 1984, Nagasawa et al 1997, White et al 2001, Chan et al 2002. These findings indicate that, for some species, maternal thyroid hormones may contribute to the control of early embryonic growth and development, before the onset of fetal thyroid hormone activity (Obregon et al 2007).…”

Section: Thyroid Hormone Transporters and Receptors In Fetal Tissuesmentioning

confidence: 99%

Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

359

270

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The thyroid hormones, thyroxine (T 4 ) and triiodothyronine (T 3 ), are essential for normal growth and development of the fetus. Their bioavailability in utero depends on development of the fetal hypothalamic-pituitary-thyroid gland axis and the abundance of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive hormone. Fetal T 4 and T 3 concentrations are also affected by gestational age, nutritional and endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). By regulating tissue accretion and differentiation near term, fetal thyroid hormones ensure activation of physiological processes essential for survival at birth such as pulmonary gas exchange, thermogenesis, hepatic glucogenesis, and cardiac adaptations. This review examines the developmental control of fetal T 4 and T 3 bioavailability and discusses the role of these hormones in fetal growth and development with particular emphasis on maturation of somatic tissues critical for survival immediately at birth.

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“…In the rat, D2 expression is first detectable at E16.5 and increases successively until postnatal day 15. Ontogenic profiling of D2 in the fetal human brain revealed the occurrence of D2 in the developing cerebral cortex during the first trimester of pregnancy just at a time point when also the cortical T3 concentration can first be detected (Chan et al, 2002). The similar ontogenic profile of D2 expression and T3 content in different developing brain structures has led to the hypothesis that D2 is particularly important in providing developing brain structures with T3 produced from maternally derived T4.…”

Section: Metabolism Of Thyroid Hormones By Brain Deiodinasesmentioning

confidence: 99%