Evidence map›Paper›PMID 32472193›Full record

ArticleDiabetologia2020

Maternal hypothyroidism in mice influences glucose metabolism in adult offspring.

Yasmine Kemkem, Daniela Nasteska, Anne de Bray, Paula Bargi-Souza, Rodrigo A Peliciari-Garcia, Anne Guillou, Patrice Mollard, David J Hodson, Marie Schaeffer

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Review
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  9. Ameliorative Effects ofNutrients · 2022
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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

9 authors at 4 institutions in 3 countries.

Yasmine KemkemInstitute of Functional Genomics, CNRS, Inserm U1191, University of Montpellier, F-34094, Montpellier, France.
Daniela NasteskaInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, UK.ORCID 0000-0002-8996-5102
Anne de BrayInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, UK.
Paula Bargi-SouzaDepartment of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Rodrigo A Peliciari-GarciaMorphophysiology and Pathology Sector, Department of Biological Sciences, Federal University of São Paulo, Diadema, SP, Brazil.
Anne GuillouInstitute of Functional Genomics, CNRS, Inserm U1191, University of Montpellier, F-34094, Montpellier, France.
Patrice MollardInstitute of Functional Genomics, CNRS, Inserm U1191, University of Montpellier, F-34094, Montpellier, France.
David J HodsonInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, UK.ORCID 0000-0002-8641-8568
Marie SchaefferInstitute of Functional Genomics, CNRS, Inserm U1191, University of Montpellier, F-34094, Montpellier, France. Marie.Schaeffer@igf.cnrs.fr.ORCID 0000-0002-2063-5324
Centre National de la Recherche Scientifique · FRUniversity of Nottingham · GBUniversidade Federal de Minas Gerais · BRUniversidade Federal de São Paulo · BR

Funding

Diabetes UK 12/0004431Diabetes UK 17/0005681Medical Research Council MR/N00275X/1Medical Research Council MR/S025618/1Wellcome Trust
6 · The paper itself

Abstract

aims/hypothesisDuring pregnancy, maternal metabolic disease and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offspring remains poorly understood.

methodsWe investigated this using a mouse model of hypothyroidism, induced by administration of an iodine-deficient diet supplemented with propylthiouracil during gestation.

resultsHere, we show that, when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation (two- to threefold increase in Ki67-positive beta cells) and increased insulin sensitivity. However, following 8 weeks of high-fat feeding, these offspring gained 20% more body weight, became profoundly hyperinsulinaemic (with a 50% increase in fasting insulin concentration), insulin-resistant and glucose-intolerant compared with controls from euthyroid mothers. Furthermore, altered glucose metabolism was maintained in a second generation of animals. CONCLUSIONS/

interpretationTherefore, gestational hypothyroidism induces long-term alterations in endocrine pancreas function, which may have implications for type 2 diabetes prevention in affected individuals.

Indexed as

AnimalsAntithyroid AgentsBlood GlucoseCell ProliferationDiet, High-FatDisease Models, AnimalFemaleGlucose IntoleranceHyperinsulinismHypothyroidismInsulin ResistanceInsulin-Secreting CellsIodineIslets of LangerhansMicePregnancyAntithyroid AgentsBlood GlucoseIodinePropylthiouracilBeta cell functionCalcium imagingDiabetesHypothyroidismPancreas

Identifiers

PMID32472193
PMCPMC7406527
OpenAlexW3031691096

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.