Evidence map›Paper›PMID 15695245›Full record

ReviewThe Journal of physiology2005

Experimental models of developmental programming: consequences of exposure to an energy rich diet during development.

James A Armitage, Paul D Taylor, Lucilla Poston

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
26.8field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 377 citations in OpenAlex.

  1. Pooled it
  2. Chromatographic Analyses of SpirulinaMedicina (Kaunas, Lithuania) · 2023
    Article
  3. Review
  4. The social formation of fitness: lifetime consequences of prenatal nutrition and postnatal care in a wild mammal population.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
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  15. Review
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  17. High-fat diet in pregnant rats and adverse fetal outcome.Upsala journal of medical sciences · 2019
    Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

James A ArmitageMaternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology and Development, GKT School of Medicine, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. james.armitage@kcl.ac.uk
Paul D Taylor
Lucilla Poston
St Thomas' Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies in both humans and experimental animals addressing the 'Fetal Origins of Adult Disease' hypothesis have established a relationship between an adverse intrauterine environment and offspring disease in adult life. This phenomenon, termed 'fetal programming' describes a process whereby a stimulus in utero establishes a permanent response in the fetus leading to enhanced susceptibility to later disease. However, the environment, during periods of developmental plasticity in postnatal life, can also 'programme' function. Thus, the terms 'developmental programming' and the 'Developmental Origins of Adult Health and Disease' are preferentially utilized. The 'Thrifty Phenotype' hypothesis explained the association between insufficient in utero nutrition and the later development of Type 2 diabetes. Most recently the 'Predictive Adaptive Response' hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is an important determinant of subsequent disease. Epidemiological studies have indicated that fetal growth restriction correlates with later disease, implying that fetal nutritional deprivation is a strong programming stimulus. This prompted the development of experimental animal models using controlled maternal calorie, protein or macronutrient deficiency during key periods of gestation. However, in many societies, maternal and postnatal nutrition are either sufficient or excessive. Here, we examine findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess. There is supportive evidence from a limited number of studies to test the 'Predictive Adaptive Response' hypothesis. These suggest that maternal over-nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.

Indexed as

Energy MetabolismPrenatal Exposure Delayed EffectsPrenatal Nutritional Physiological PhenomenaAdaptation, PhysiologicalAnimalsCardiovascular SystemDietDisease Models, AnimalFemaleHumansMaternal ExposureMetabolic SyndromeModels, AnimalModels, BiologicalObesityPregnancy

Identifiers

PMID15695245
PMCPMC1464498
OpenAlexW1563149938

What OpenQuestion holds

Textmetadata
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.