Evidence map›Paper›PMID 20573724›Full record

ArticleEndocrinology2010

Perinatal iron and copper deficiencies alter neonatal rat circulating and brain thyroid hormone concentrations.

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

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

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  8. Reducing uncertainties in quantitative adverse outcome pathways by analysis of thyroid hormone in the neonatal rat brain.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
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  17. Article
  18. Article
  19. Iron assessment to protect the developing brain.The American journal of clinical nutrition · 2017
    Review
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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 2 institutions in 1 country.

Thomas W BastianDepartment of Pharmacy Practice and Pharmaceutical Sciences, College of Pharmacy, University of Minnesota Duluth, Duluth, Minnesota 55812, USA.
Joseph R Prohaska
Michael K Georgieff
Grant W Anderson
University of Minnesota, Duluth · USUniversity of Minnesota · US

Funding

NEWBORN IRON DEFICIENCYR01HD029421 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI GEORGIEFF, MICHAEL K. · 2000 to 2015
$4.4M
NUTRITIONAL COPPER STATUS AND THE NERVOUS SYSTEMR01HD039708 · NICHD · UNIVERSITY OF MINNESOTA DULUTH · PI PROHASKA, JOSEPH ROBERT · 2001 to 2010
$1.5M
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 R01 HD039708NICHD NIH HHS R01HD039708-08NICHD NIH HHS R01 HD29421-15NICHD NIH HHS R03 HD055423
6 · The paper itself

Abstract

Copper (Cu), iron (Fe), and iodine/thyroid hormone (TH) deficiencies lead to similar defects in late brain development, suggesting that these micronutrient deficiencies share a common mechanism contributing to the observed derangements. Previous studies in rodents (postweanling and adult) and humans (adolescent and adult) indicate that Cu and Fe deficiencies affect the hypothalamic-pituitary-thyroid axis, leading to altered TH status. Importantly, however, relationships between Fe and Cu deficiencies and thyroidal status have not been assessed in the most vulnerable population, the developing fetus/neonate. We hypothesized that Cu and Fe deficiencies reduce circulating and brain TH levels during development, contributing to the defects in brain development associated with these deficiencies. To test this hypothesis, pregnant rat dams were rendered Cu deficient (CuD), FeD, or TH deficient from early gestation through weaning. Serum thyroxine (T(4)) and triiodothyronine (T(3)), and brain T(3) levels, were subsequently measured in postnatal d 12 (P12) pups. Cu deficiency reduced serum total T(3) by 48%, serum total T(4) by 21%, and whole-brain T(3) by 10% at P12. Fe deficiency reduced serum total T(3) by 43%, serum total T(4) by 67%, and whole-brain T(3) by 25% at P12. Brain mRNA analysis revealed that expression of several TH-responsive genes were altered in CuD or FeD neonates, suggesting that reduced TH concentrations were sensed by the FeD and CuD neonatal brain. These results indicate that at least some of the brain defects associated with neonatal Fe and Cu deficiencies are mediated through reductions in circulating and brain TH levels.

Indexed as

Iron DeficienciesAnimalsAnimals, NewbornBrainCopperDeficiency DiseasesFemaleGene Expression Regulation, DevelopmentalIronMalePregnancyPropylthiouracilRatsRats, Sprague-DawleyRNA, MessengerThyroid GlandCopperIronPropylthiouracilRNA, MessengerThyroid Hormones

Identifiers

PMID20573724
PMCPMC2940517
OpenAlexW2044120323

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.