Evidence map›Paper›PMID 32494846›Full record

ReviewCellular and molecular life sciences : CMLS2020

Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress.

Efthimia R Christoforou, Amanda N Sferruzzi-Perri

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
10.8field-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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Transient fetal hyperglycemia reprograms adipogenesis, lipogenesis, and insulin signaling in zebrafish.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Article
  3. Distinct Effects of Maternal Stress and Exercise on Offspring Metabolic Health.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
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  10. Maternal Nutrition, Toxicants, and Epigenetic Programming of Obesity Across Generations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
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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.

Efthimia R ChristoforouDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Downing Site, Cambridge, UK.
Amanda N Sferruzzi-PerriDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Downing Site, Cambridge, UK. ans48@cam.ac.uk.ORCID http://orcid.org/0000-0002-4931-4233
University of Cambridge · GB

Funding

Lister Institute of Preventive Medicine RG93692Medical Research Council MR/R022690/1Medical Research Council (UK) RG93186Royal Society RG74249
6 · The paper itself

Abstract

The results of different human epidemiological datasets provided the impetus to introduce the now commonly accepted theory coined as 'developmental programming', whereby the presence of a stressor during gestation predisposes the growing fetus to develop diseases, such as metabolic dysfunction in later postnatal life. However, in a clinical setting, human lifespan and inaccessibility to tissue for analysis are major limitations to study the molecular mechanisms governing developmental programming. Subsequently, studies using animal models have proved indispensable to the identification of key molecular pathways and epigenetic mechanisms that are dysregulated in metabolic organs of the fetus and adult programmed due to an adverse gestational environment. Rodents such as mice and rats are the most used experimental animals in the study of developmental programming. This review summarises the molecular pathways and epigenetic mechanisms influencing alterations in metabolic tissues of rodent offspring exposed to in utero stress and subsequently programmed for metabolic dysfunction. By comparing molecular mechanisms in a variety of rodent models of in utero stress, we hope to summarise common themes and pathways governing later metabolic dysfunction in the offspring whilst identifying reasons for incongruencies between models so to inform future work. With the continued use and refinement of such models of developmental programming, the scientific community may gain the knowledge required for the targeted treatment of metabolic diseases that have intrauterine origins.

Indexed as

Disease Models, AnimalMetabolismStress, PhysiologicalAnimalsEpigenesis, GeneticInsulinLiverRodentiaInsulinAnimal modelsDevelopmentDOHADFetalMetabolismProgramming

Identifiers

PMID32494846
PMCPMC7658077
OpenAlexW3030004809

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.