Evidence map›Paper›PMID 23152876›Full record

ArticlePloS one2012

High fat diet induced developmental defects in the mouse: oocyte meiotic aneuploidy and fetal growth retardation/brain defects.

Kerri M Luzzo, Qiang Wang, Scott H Purcell, Maggie Chi, Patricia T Jimenez, Natalia Grindler, Tim Schedl, Kelle H Moley

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 1 pooled it
32.4field-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

159 citing papers in PubMed, 1 synthesis or guideline pooled it, 353 citations in OpenAlex.

  1. Pooled it
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  10. Mitochondrial dysfunction in pregnancy loss: a review.Molecular and cellular biochemistry · 2025
    Review
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99 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Kerri M LuzzoWashington University School of Medicine, Department of Obstetrics and Gynecology, St. Louis, Missouri, United States of America.
Qiang Wang
Scott H Purcell
Maggie Chi
Patricia T Jimenez
Natalia Grindler
Tim Schedl
Kelle H Moley
Washington University in St. Louis · USNanjing Medical University · CN

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
A National Training Program in Reproductive MedicineT32HD040135 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI COUTIFARIS, CHRISTOS · 2002 to 2016
$3.6M
GLUTS AND GLUCOSE TRANSPORT IN THE MOUSE BLASTOCYSTR01HD040390 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2012
$2.6M
Training in Reproductive SciencesT32HD049305 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2005 to 2015
$1.9M
MPK -1 ERK SUBSTRATES AND THE CONTROL OF GERMLINE DEVELOPMENTR01GM085150 · NIGMS · WASHINGTON UNIVERSITY · PI SCHEDL, TIM · 2008 to 2011
$1.3M
NICHD NIH HHS HD40390NICHD NIH HHS R01 HD040390NICHD NIH HHS T32 HD040135NICHD NIH HHS T32 HD049305NIDDK NIH HHS P30 DK020579NIGMS NIH HHS R01 GM085150
6 · The paper itself

Abstract

backgroundMaternal obesity is associated with poor outcomes across the reproductive spectrum including infertility, increased time to pregnancy, early pregnancy loss, fetal loss, congenital abnormalities and neonatal conditions. Furthermore, the proportion of reproductive-aged woman that are obese in the population is increasing sharply. From current studies it is not clear if the origin of the reproductive complications is attributable to problems that arise in the oocyte or the uterine environment. METHODOLOGY/PRINCIPAL

findingsWe examined the developmental basis of the reproductive phenotypes in obese animals by employing a high fat diet mouse model of obesity. We analyzed very early embryonic and fetal phenotypes, which can be parsed into three abnormal developmental processes that occur in obese mothers. The first is oocyte meiotic aneuploidy that then leads to early embryonic loss. The second is an abnormal process distinct from meiotic aneuploidy that also leads to early embryonic loss. The third is fetal growth retardation and brain developmental abnormalities, which based on embryo transfer experiments are not due to the obese uterine environment but instead must be from a defect that arises prior to the blastocyst stage. CONCLUSIONS/SIGNIFICANCE: Our results suggest that reproductive complications in obese females are, at least in part, from oocyte maternal effects. This conclusion is consistent with IVF studies where the increased pregnancy failure rate in obese women returns to the normal rate if donor oocytes are used instead of autologous oocytes. We postulate that preconceptional weight gain adversely affects pregnancy outcomes and fetal development. In light of our findings, preconceptional counseling may be indicated as the preferable, earlier target for intervention in obese women desiring pregnancy and healthy outcomes.

Indexed as

AneuploidyMeiosisAnimalsBrainChromosomes, MammalianCumulus CellsDiet, High-FatEmbryo, MammalianFeeding BehaviorFemaleFetal DevelopmentFetal Growth RetardationHumansMiceMice, Inbred ICRMitochondria

Identifiers

PMID23152876
PMCPMC3495769
OpenAlexW2071592190

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.