Evidence map›Paper›PMID 22047985›Full record

ArticleMedical hypotheses2012

A common cause for a common phenotype: the gatekeeper hypothesis in fetal programming.

S McMullen, S C Langley-Evans, L Gambling, C Lang, A Swali, H J McArdle

Abstract read
In one paragraph

Article in Medical hypotheses, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

  1. Article
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  8. Review
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  11. Review
  12. Metabolic programming in early life in humans.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Developmental Programming of Adult Disease: Reprogramming by Melatonin?International journal of molecular sciences · 2017
    Review
  17. Review
  18. Article
  19. Review
  20. Review
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

6 authors.

S McMullenSchool of Biosciences, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, UK.
S C Langley-Evans
L Gambling
C Lang
A Swali
H J McArdle

Funding

Biotechnology and Biological Sciences Research Council BB/F005245/1
6 · The paper itself

Abstract

Sub-optimal nutrition during pregnancy has been shown to have long-term effects on the health of offspring in both humans and animals. The most common outcomes of such programming are hypertension, obesity, dyslipidaemia and insulin resistance. This spectrum of disorders, collectively known as metabolic syndrome, appears to be the consequence of nutritional insult during early development, irrespective of the nutritional stress experienced. For example, diets low in protein diet, high in fat, or deficient in iron are all associated with programming of cardiovascular and metabolic disorders when fed during rat pregnancy. In this paper, we hypothesise that the nutritional stresses act on genes or gene pathways common to all of the insults. We have termed these genes and/or gene pathways the "gatekeepers" and hence developed the "gatekeeper hypothesis". In this paper, we examine the background to the hypothesis and postulate some possible mechanisms or pathways that may constitute programming gatekeepers.

Indexed as

Models, BiologicalAdaptation, BiologicalAnimalsEpigenesis, GeneticFemaleFetal Nutrition DisordersHumansMetabolic SyndromePregnancyPrenatal Exposure Delayed EffectsRatsScandinavian and Nordic CountriesSignal TransductionUnited States

Identifiers

PMID22047985
PMCPMC3426771

What OpenQuestion holds

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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.