Evidence map›Paper›PMID 29391475›Full record

ArticleScientific reports2018

Periconception onset diabetes is associated with embryopathy and fetal growth retardation, reproductive tract hyperglycosylation and impaired immune adaptation to pregnancy.

Hannah M Brown, Ella S Green, Tiffany C Y Tan, Macarena B Gonzalez, Alice R Rumbold, M Louise Hull, Robert J Norman, Nicolle H Packer, Sarah A Robertson, Jeremy G Thompson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

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  9. Effects of Peri-Conception and Pregnancy Glycemic Variability on Pregnancy and Perinatal Complications in Type 1 Diabetes: A Pilot Study.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022
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  17. Frontiers in physiology · 2018
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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

10 authors at 3 institutions in 1 country.

Hannah M BrownRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia. Hannah.brown@adelaide.edu.au.ORCID http://orcid.org/0000-0001-6342-3316
Ella S GreenRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Tiffany C Y TanRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Macarena B GonzalezRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Alice R RumboldRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
M Louise HullRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Robert J NormanRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Nicolle H PackerARC Centre for Nanoscale Biophotonics, Department of Molecular Sciences, Macquarie University, Sydney, Australia.
Sarah A RobertsonRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
Jeremy G ThompsonRobinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, Australia.
The University of Adelaide · AUAustralian Research Council · AUMacquarie University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes has been linked with impaired fertility but the underlying mechanisms are not well defined. Here we use a streptozotocin-induced diabetes mouse model to investigate the cellular and biochemical changes in conceptus and maternal tissues that accompany hyperglycaemia. We report that streptozotocin treatment before conception induces profound intra-cellular protein β-O-glycosylation (O-GlcNAc) in the oviduct and uterine epithelium, prominent in early pregnancy. Diabetic mice have impaired blastocyst development and reduced embryo implantation rates, and delayed mid-gestation growth and development. Peri-conception changes are accompanied by increased expression of pro-inflammatory cytokine Trail, and a trend towards increased Il1a, Tnf and Ifng in the uterus, and changes in local T-cell dynamics that skew the adaptive immune response to pregnancy, resulting in 60% fewer anti-inflammatory regulatory T-cells within the uterus-draining lymph nodes. Activation of the heat shock chaperones, a mechanism for stress deflection, was evident in the reproductive tract. Additionally, we show that the embryo exhibits elevated hyper-O-GlcNAcylation of both cytoplasmic and nuclear proteins, associated with activation of DNA damage (ɣH2AX) pathways. These results advance understanding of the impact of peri-conception diabetes, and provide a foundation for designing interventions to support healthy conception without propagation of disease legacy to offspring.

Indexed as

FertilizationAnimalsDiabetes Mellitus, ExperimentalEmbryo, MammalianEmbryonic DevelopmentFemaleFetal Growth RetardationGlycosylationMiceMice, Inbred C57BLPregnancyPregnancy ComplicationsPregnancy in DiabeticsReproductionUterus

Identifiers

PMID29391475
PMCPMC5794861
OpenAlexW2807001102

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.