Evidence map›Paper›PMID 32221393›Full record

ArticleScientific reports2020

Inner histopathologic changes and disproportionate zone volumes in foetal growth plates following gestational hypoglycaemia in rats.

Vivi F H Jensen, Anne-Marie Mølck, Ingrid B Bøgh, Jette Nowak, Birgitte M Viuff, Charlotte L M Rasmussen, Louise Pedersen, Johannes J Fels, Suzi H Madsen, Fiona E McGuigan and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 64% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

13 authors at 3 institutions in 2 countries.

Vivi F H JensenNovo Nordisk A/S, Department of Toxicology, Safety Pharmacology and Pathology, Maaloev, Denmark. vfhj@novonordisk.com.
Anne-Marie MølckNovo Nordisk A/S, Department of Toxicology, Safety Pharmacology and Pathology, Maaloev, Denmark.
Ingrid B BøghNovo Nordisk A/S, Department of Toxicology, Safety Pharmacology and Pathology, Maaloev, Denmark.
Jette NowakNovo Nordisk A/S, Department of Toxicology, Safety Pharmacology and Pathology, Maaloev, Denmark.
Birgitte M ViuffNovo Nordisk A/S, Department of Toxicology, Safety Pharmacology and Pathology, Maaloev, Denmark.
Charlotte L M RasmussenUniversity of Copenhagen, Department of Veterinary and Animal Sciences, Section for Experimental Animal Models, Copenhagen, Denmark.
Louise PedersenUniversity of Copenhagen, Department of Veterinary and Animal Sciences, Section for Experimental Animal Models, Copenhagen, Denmark.
Johannes J FelsNovo Nordisk A/S, Department of Research Bioanalysis, Maaloev, Denmark.
Suzi H MadsenNovo Nordisk A/S, Department of Research Bioanalysis, Maaloev, Denmark.
Fiona E McGuiganLund University, Department of Clinical Sciences Malmö and Skåne University Hospital, Department of Orthopedics, Malmö, Sweden.
Pernille Tveden-NyborgUniversity of Copenhagen, Department of Veterinary and Animal Sciences, Section for Experimental Animal Models, Copenhagen, Denmark.
Jens LykkesfeldtUniversity of Copenhagen, Department of Veterinary and Animal Sciences, Section for Experimental Animal Models, Copenhagen, Denmark.
Kristina E AkessonLund University, Department of Clinical Sciences Malmö and Skåne University Hospital, Department of Orthopedics, Malmö, Sweden.
Novo Nordisk (Denmark) · DKUniversity of Copenhagen · DKLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal hypoglycaemia throughout gestation until gestation day (GD)20 delays foetal growth and skeletal development. While partially prevented by return to normoglycaemia after completed organogenesis (GD17), underlying mechanisms are not fully understood. Here, we investigated the pathogenesis of these changes and significance of maternal hypoglycaemia extending beyond organogenesis in non-diabetic rats. Pregnant rats received insulin-infusion until GD20 or GD17, with sacrifice on GD20. Hypoglycaemia throughout gestation increased maternal corticosterone levels, which correlated with foetal levels. Growth plates displayed central histopathologic changes comprising disrupted cellular organisation, hypertrophic chondrocytes, and decreased cellular density; expression of pro-angiogenic factors, HIF-1α and VEGF-A increased in surrounding areas. Disproportionately decreased growth plate zone volumes and lower expression of the structural protein MATN-3 were seen, while bone ossification parameters were normal. Ending maternal/foetal hypoglycaemia on GD17 reduced incidence and severity of histopathologic changes and with normal growth plate volume. Compromised foetal skeletal development following maternal hypoglycaemia throughout gestation is hypothesised to result from corticosterone-induced hypoxia in growth plates, where hypoxia disrupts chondrocyte maturation and growth plate structure and volume, decreasing long bone growth. Maternal/foetal hypoglycaemia lasting only until GD17 attenuated these changes, suggesting a pivotal role of glucose in growth plate development.

Indexed as

AnimalsCell DifferentiationChondrocytesCorticosteroneFemaleFetal DevelopmentFetusGrowth PlateHypoglycemiaHypoxiaHypoxia-Inducible Factor 1, alpha SubunitNeovascularization, PathologicPregnancyPrenatal CareRatsRats, Sprague-DawleyCorticosteroneHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor A

Identifiers

PMID32221393
PMCPMC7101337
OpenAlexW3013824181

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.