Evidence map›Paper›PMID 28916763›Full record

ArticleScientific reports2017

Maternal diabetes causes developmental delay and death in early-somite mouse embryos.

Jing Zhao, Theodorus B M Hakvoort, Jan M Ruijter, Aldo Jongejan, Jan Koster, Sigrid M A Swagemakers, Aleksandar Sokolovic, Wouter H Lamers

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

  1. Article
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  10. 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

8 authors at 3 institutions in 1 country.

Jing ZhaoTytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, Netherlands.
Theodorus B M HakvoortTytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, Netherlands.
Jan M RuijterDepartment of Anatomy, Embryology & Physiology, AMC, Amsterdam, Netherlands.
Aldo JongejanBioinformatics Laboratory, Department of Clinical Epidemiology, Biostatistics & Bioinformatics, AMC, Amsterdam, Netherlands.
Jan KosterDepartment of Oncogenomics, AMC, Amsterdam, Netherlands.
Sigrid M A SwagemakersDepartment of Informatics, Erasmus Medical Center, Rotterdam, Netherlands.
Aleksandar SokolovicTytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, Netherlands.
Wouter H LamersTytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, Netherlands. w.h.lamers@amc.uva.nl.ORCID 0000-0003-3032-7824
Amsterdam UMC Location University of Amsterdam · NLErasmus MC · NLNetherlands Bioinformatics Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal diabetes causes congenital malformations and delays embryonic growth in the offspring. We investigated effects of maternal diabetes on mouse embryos during gastrulation and early organogenesis (ED7.5-11.5). Female mice were made diabetic with streptozotocin, treated with controlled-release insulin implants, and mated. Maternal blood glucose concentrations increased up to embryonic day (ED) 8.5. Maternal hyperglycemia induced severe growth retardation (approx.1 day) in 53% of the embryos on ED8.5, death in most of these embryos on ED9.5, and the termination of pregnancy on ED10.5 in litters with >20% dead embryos. Due to this selection, developmental delays and reduction in litter size were no longer observed thereafter in diabetic pregnancies. Male and female embryos were equally sensitive. High-throughput mRNA sequencing and pathway analysis of differentially expressed genes showed that retarded embryos failed to mount the adaptive suppression of gene expression that characterized non-retarded embryos (cell proliferation, cytoskeletal remodeling, oxidative phosphorylation). We conclude that failure of perigastrulation embryos of diabetic mothers to grow and survive is associated with their failure to shut down pathways that are strongly down-regulated in otherwise similar non-retarded embryos. Embryos that survive the early and generalized adverse effect of maternal diabetes, therefore, appear the subset in which malformations become manifest.

Indexed as

Pregnancy in DiabeticsAnimalsCongenital AbnormalitiesDevelopmental DisabilitiesDiabetes Mellitus, ExperimentalEmbryo LossEmbryo, MammalianFemaleLitter SizeMicePregnancySomitesStreptozocinStreptozocin

Identifiers

PMID28916763
PMCPMC5601907
OpenAlexW2754179407

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.