Evidence map›Paper›PMID 36782211›Full record

ReviewBMC medicine2023

Maternal obesity and programming of metabolic syndrome in the offspring: searching for mechanisms in the adipocyte progenitor pool.

Taylor B Scheidl, Amy L Brightwell, Sarah H Easson, Jennifer A Thompson

Open access · goldAbstract readReview
In one paragraph

Review in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
25.0field-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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Beyond Deterministic Fetal Programming: Intrauterine Exposures and the Multifactorial Origins of Adiposity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
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  16. Observational
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  19. Investigating the Pathogenesis and Treatment of Type 2 Diabetes from the Perspective of Adipose Tissue.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    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

4 authors at 3 institutions in 1 country.

Taylor B ScheidlCumming School of Medicine, Calgary, Canada.
Amy L BrightwellUniversity of Calgary, 3330 Hospital Dr. NW, Calgary, AB, T2N 4N1, Canada.
Sarah H EassonCumming School of Medicine, Calgary, Canada.
Jennifer A ThompsonCumming School of Medicine, Calgary, Canada. Jennifer.thompson2@ucalgary.ca.
University of Calgary · CAAlberta Children's Hospital · CAAlberta Children's Hospital Research Institute

Funding

CIHR 162452Heart and Stroke Foundation of Canada G-19-0026536
6 · The paper itself

Abstract

backgroundIt is now understood that it is the quality rather than the absolute amount of adipose tissue that confers risk for obesity-associated disease. Adipose-derived stem cells give rise to adipocytes during the developmental establishment of adipose depots. In adult depots, a reservoir of progenitors serves to replace adipocytes that have reached their lifespan and for recruitment to increase lipid buffering capacity under conditions of positive energy balance. MAIN: The adipose tissue expandability hypothesis posits that a failure in de novo differentiation of adipocytes limits lipid storage capacity and leads to spillover of lipids into the circulation, precipitating the onset of obesity-associated disease. Since adipose progenitors are specified to their fate during late fetal life, perturbations in the intrauterine environment may influence the rapid expansion of adipose depots that occurs in childhood or progenitor function in established adult depots. Neonates born to mothers with obesity or diabetes during pregnancy tend to have excessive adiposity at birth and are at increased risk for childhood adiposity and cardiometabolic disease.

conclusionIn this narrative review, we synthesize current knowledge in the fields of obesity and developmental biology together with literature from the field of the developmental origins of health and disease (DOHaD) to put forth the hypothesis that the intrauterine milieu of pregnancies complicated by maternal metabolic disease disturbs adipogenesis in the fetus, thereby accelerating the trajectory of adipose expansion in early postnatal life and predisposing to impaired adipose plasticity.

Indexed as

Metabolic SyndromePediatric ObesityPregnancy in ObesityAdipocytesAdipose TissueAdultFemaleHumansInfant, NewbornLipidsPregnancyLipidsAdipose tissueFetal programmingGestational diabetesMetabolic syndromeObesity

Identifiers

PMID36782211
PMCPMC9924890
OpenAlexW4320482277

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.