Evidence map›Paper›PMID 20564432›Full record

ArticleBirth defects research. Part A, Clinical and molecular teratology2010

Neural tube defect genes and maternal diabetes during pregnancy.

J Michael Salbaum, Claudia Kappen

Open access · greenAbstract read
In one paragraph

Article in Birth defects research. Part A, Clinical and molecular teratology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Observational
  14. Epigenetic Changes in Gestational Diabetes Mellitus.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

J Michael SalbaumLaboratory of Regulation of Gene Expression, 6400 Perkins Road, Baton Rouge, Louisiana 70808, USA. michael.salbaum@pbrc.edu
Claudia Kappen
Pennington Biomedical Research Center · US

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2005 to 2026
$26.5M
MOLECULAR MECHANISMS IN DIABETIC EMBRYOPATHYR01HD037804 · NICHD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KAPPEN, CLAUDIA T · 1998 to 2010
$2.5M
Neural tube defects in diabetic pregnancyR01HD055528 · NICHD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI SALBAUM, J MICHAEL · 2007 to 2011
$1.8M
NICHD NIH HHS R01 HD037804NICHD NIH HHS R01 HD055528NICHD NIH HHS R01HD055528NICHD NIH HHS R01HD37804NIDDK NIH HHS P30 DK072476
6 · The paper itself

Abstract

backgroundMaternal diabetes during pregnancy is a well-known teratogen that increases the risk for birth defects, such as neural tube defects (NTDs). We have previously shown that maternal diabetes profoundly affects gene expression in the developing embryo, in particular a suite of known NTD genes. In rodent experimental systems, NTDs present as phenotypes of incomplete penetrance in diabetic pregnancies. This property is difficult to reconcile with observations of consistently altered gene expression in exposed embryos. We here show that maternal diabetes increases the overall variability of gene expression levels in embryos.

resultsAltered gene expression and increased variability of gene expression together may constitute the molecular correlates for incomplete phenotype penetrance. DISCUSSION: Based on this model, we suggest that maternal diabetes reduces the precision of gene regulation in exposed individuals. Loss of precision in embryonic gene regulation may include changes to the epigenome via deregulated expression of chromatin-modifying factors. Unraveling the mechanisms underlying such epigenetic modifications in diabetic pregnancies will help to understand how teratogenic insults compromise embryonic development and possibly provide avenues for therapeutic intervention.

Indexed as

Gene ExpressionGene Expression Regulation, DevelopmentalAnimalsDiabetes, GestationalFemaleGene Expression ProfilingGenetic VariationHumansKidneyMiceNeural Tube DefectsPlacentaPregnancyTranscription FactorsTranscription, GeneticTranscription Factors

Identifiers

PMID20564432
PMCPMC3509193
OpenAlexW2094796994

What OpenQuestion holds

Textmetadata
LicenceTDM
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.