ArticleEndocrinology2012
Fetal and neonatal iron deficiency reduces thyroid hormone-responsive gene mRNA levels in the neonatal rat hippocampus and cerebral cortex.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Cellular Iron Deficiency Disrupts Thyroid Hormone Regulated Gene Expression in Developing Hippocampal Neurons.The Journal of nutrition · 2024Article
- Refractory thrombocytopenia could be a rare initial presentation of Noonan syndrome in newborn infants: a case report and literature review.BMC pediatrics · 2022Review
- Thyroid Disruptors: Extrathyroidal Sites of Chemical Action and Neurodevelopmental Outcome-An Examination Using Triclosan and Perfluorohexane Sulfonate.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Infantile Iron Deficiency Affects Brain Development in Monkeys Even After Treatment of Anemia.Frontiers in human neuroscience · 2021Article
- Thyroid disrupting chemicals and developmental neurotoxicity - New tools and approaches to evaluate hormone action.Molecular and cellular endocrinology · 2020Review
- Regulation of Thyroid-disrupting Chemicals to Protect the Developing Brain.Endocrinology · 2020Review
- Evaluating thyroid hormone disruption: investigations of long-term neurodevelopmental effects in rats after perinatal exposure to perfluorohexane sulfonate (PFHxS).Scientific reports · 2020Article
- The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism.Neuroscience insights · 2020Review
- Thyroid Hormone Disruption in the Fetal and Neonatal Rat: Predictive Hormone Measures and Bioindicators of Hormone Action in the Developing Cortex.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Review
- Chronic anemia and thyroid function.Acta bio-medica : Atenei Parmensis · 2017Review
- Adult hippocampal neurogenesis is impaired by transient and moderate developmental thyroid hormone disruption.Neurotoxicology · 2017Article
- Thyroxine administration prevents matrilineal intergenerational consequences of in utero ethanol exposure in rats.Hormones and behavior · 2016Article
- Evaluation of the effects of serum iron levels on lacrimal gland secretion.The Kaohsiung journal of medical sciences · 2015Article
- Maternal Iron Status in Pregnancy and Long-Term Health Outcomes in the Offspring.Journal of pediatric genetics · 2015Review
- Fetal and neonatal iron deficiency but not copper deficiency increases vascular complexity in the developing rat brain.Nutritional neuroscience · 2015Article
- Gestational iron deficiency differentially alters the structure and function of white and gray matter brain regions of developing rats.The Journal of nutrition · 2014Article
- Fetal and neonatal iron deficiency exacerbates mild thyroid hormone insufficiency effects on male thyroid hormone levels and brain thyroid hormone-responsive gene expression.Endocrinology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Copper (Cu), iron (Fe), and thyroid hormone (TH) deficiencies produce similar defects in late brain development including hypomyelination of axons and impaired synapse formation and function, suggesting that these micronutrient deficiencies share a common mechanism contributing to these derangements. We previously demonstrated that fetal/neonatal Cu and Fe deficiencies lower circulating TH concentrations in neonatal rats. Fe deficiency also reduces whole-brain T(3) content, suggesting impaired TH action in the developing Fe-deficient brain. We hypothesized that fetal/neonatal Cu and Fe deficiencies will produce mild or moderate TH deficiencies and will impair TH-responsive gene expression in the neonatal cerebral cortex and hippocampus. To test this hypothesis, we rendered pregnant Sprague Dawley rats Cu-, Fe-, or TH-deficient from early gestation through postnatal d 10 (P10). Mild and moderate TH deficiencies were induced by 1 and 3 ppm propylthiouracil treatment, respectively. Cu deficiency did not significantly alter serum or tissue TH concentrations or TH-responsive brain mRNA expression. Fe deficiency significantly lowered P10 serum total T(3) (45%), serum total T(4) (52%), whole brain T(3) (14%), and hippocampal T(3) (18%) concentrations, producing a mild TH deficiency similar to 1 ppm propylthiouracil treatment. Fe deficiency lowered Pvalb, Enpp6, and Mbp mRNA levels in the P10 hippocampus. Fe deficiency also altered Hairless, Dbm, and Dio2 mRNA levels in the P10 cerebral cortex. These results suggest that some of the brain defects associated with Fe deficiency may be mediated through altered thyroidal status and the concomitant alterations in TH-responsive gene transcription.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.