Evidence map›Paper›PMID 23820120›Full record

ReviewClinical obstetrics and gynecology2013

Prenatal programming of insulin secretion in intrauterine growth restriction.

Kathryn L Gatford, Rebecca A Simmons

Open access · greenAbstract readReview
In one paragraph

Review in Clinical obstetrics and gynecology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.9field-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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  8. Article
  9. Review
  10. Review
  11. Article
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  13. Article
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  15. Article
  16. Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2019
    Review
  17. Article
  18. Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Review
  19. Article
  20. 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

2 authors at 2 institutions in 2 countries.

Kathryn L GatfordRobinson Institute, and School of Paediatrics and Reproductive Health, University of Adelaide, SA, Australia, USA. kathy.gatford@adelaide.edu.au
Rebecca A Simmons
University of Adelaide · AUUniversity of Washington · US

Funding

MECHANISMS BY WHICH IUGR LEADS TO DIABETESR01DK055704 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SIMMONS, REBECCA A · 2000 to 2014
$3.6M
NIDDK NIH HHS R01 DK055704
6 · The paper itself

Abstract

Intrauterine growth restriction (IUGR) impairs insulin secretion in humans and in animal models of IUGR. Several underlying mechanisms have been implicated, including decreased expression of molecular regulators of β-cell mass and function, in some cases shown to be due to epigenetic changes initiated by an adverse fetal environment. Alterations in cell cycle progression contribute to loss of β-cell mass, whereas decreased islet vascularity and mitochondrial dysfunction impair β-cell function in IUGR rodents. Animal models of IUGR sharing similar insulin secretion outcomes as the IUGR human are allowing underlying mechanisms to be identified. This review will focus on models of uteroplacental insufficiency.

Indexed as

AnimalsDiabetes Mellitus, Type 2Epigenesis, GeneticFemaleFetal DevelopmentFetal Growth RetardationFetusHumansInsulinInsulin-Secreting CellsInsulin SecretionPregnancyInsulin

Identifiers

PMID23820120
PMCPMC4095881
OpenAlexW2006599836

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.