Evidence map›Paper›PMID 24424046›Full record

ArticleEndocrinology2014

Fetal and neonatal iron deficiency exacerbates mild thyroid hormone insufficiency effects on male thyroid hormone levels and brain thyroid hormone-responsive gene expression.

Thomas W Bastian, Joseph R Prohaska, Michael K Georgieff, Grant W Anderson

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Deletion of Transferrin Receptor 1 in Parvalbumin Interneurons Induces a Hereditary Spastic Paraplegia-Like Phenotype.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Chronic anemia and thyroid function.Acta bio-medica : Atenei Parmensis · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Thomas W BastianDepartment of Pharmacy Practice and Pharmaceutical Sciences (T.W.B., G.W.A.), College of Pharmacy, University of Minnesota Duluth, Duluth, Minnesota 55812; Department of Biomedical Sciences (J.R.P.), University of Minnesota Medical School Duluth, Duluth, Minnesota 55812; Department of Pediatrics and Center for Neurobehavioral Development (M.K.G.), School of Medicine, University of Minnesota, Minneapolis, Minnesota 55454.
Joseph R Prohaska
Michael K Georgieff
Grant W Anderson
University of Minnesota, Duluth · USDuluth Clinic · USUniversity of Minnesota · US

Funding

NEWBORN IRON DEFICIENCYR01HD029421 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI GEORGIEFF, MICHAEL K. · 2000 to 2015
$4.4M
Copper, Iron and Thyroid Hormone Deficiency During Brain DevelopmentR03HD055423 · NICHD · UNIVERSITY OF MINNESOTA · PI ANDERSON, GRANT W, GEORGIEFF, MICHAEL K. · 2008 to 2009
$134k
NICHD NIH HHS 5R03HD055423-02NICHD NIH HHS R01 HD029421NICHD NIH HHS R03 HD055423
6 · The paper itself

Abstract

Fetal/neonatal iron (Fe) and iodine/TH deficiencies lead to similar brain developmental abnormalities and often coexist in developing countries. We recently demonstrated that fetal/neonatal Fe deficiency results in a mild neonatal thyroidal impairment, suggesting that TH insufficiency contributes to the neurodevelopmental abnormalities associated with Fe deficiency. We hypothesized that combining Fe deficiency with an additional mild thyroidal perturbation (6-propyl-2-thiouracil [PTU]) during development would more severely impair neonatal thyroidal status and brain TH-responsive gene expression than either deficiency alone. Early gestation pregnant rats were assigned to 7 different treatment groups: control, Fe deficient (FeD), mild TH deficient (1 ppm PTU), moderate TH deficient (3 ppm PTU), severe TH deficient (10 ppm PTU), FeD/1 ppm PTU, or FeD/3 ppm PTU. FeD or 1 ppm PTU treatment alone reduced postnatal day 15 serum total T4 concentrations by 64% and 74%, respectively, without significantly altering serum total T3 concentrations. Neither treatment alone significantly altered postnatal day 16 cortical or hippocampal T3 concentrations. FeD combined with 1 ppm PTU treatment produced a more severe effect, reducing serum total T4 by 95%, and lowering hippocampal and cortical T3 concentrations by 24% and 31%, respectively. Combined FeD/PTU had a more severe effect on brain TH-responsive gene expression than either treatment alone, significantly altering Pvalb, Dio2, Mbp, and Hairless hippocampal and/or cortical mRNA levels. FeD/PTU treatment more severely impacted cortical and hippocampal parvalbumin protein expression compared with either individual treatment. These data suggest that combining 2 mild thyroidal insults during development significantly disrupts thyroid function and impairs TH-regulated brain gene expression.

Indexed as

Gene Expression RegulationIron DeficienciesAnimalsBrainCerebral CortexDisease Models, AnimalFemaleGene ExpressionHippocampusMaleMaternal ExposureParvalbuminsPregnancyPropylthiouracilRadioimmunoassayRatsParvalbuminsPropylthiouracilRNA, MessengerThyroid Hormones

Identifiers

PMID24424046
PMCPMC3929725
OpenAlexW2005035568

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.