Evidence map›Paper›PMID 28122721›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

Adverse metabolic phenotype of female offspring exposed to preeclampsia in utero: a characterization of the BPH/5 mouse in postnatal life.

Elizabeth F Sutton, Heinrich E Lob, Jiunn Song, YunWei Xia, Scott Butler, Chin-Chi Liu, Leanne M Redman, Jenny L Sones

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. 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
1.9field-weighted citation impact, top 15% 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, 39 citations in OpenAlex.

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  7. Guidelines for in vivo models of developmental programming of cardiovascular disease risk.American journal of physiology. Heart and circulatory physiology · 2024
    Review
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  10. Reversal of maternal obesity attenuates hypoxia and improves placental development in the preeclamptic-like BPH/5 mouse model.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2023
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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

8 authors at 3 institutions in 1 country.

Elizabeth F SuttonPennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana.
Heinrich E LobBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York; and.
Jiunn SongBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York; and.
YunWei XiaBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York; and.
Scott ButlerBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York; and.
Chin-Chi LiuVeterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana.
Leanne M RedmanPennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana.
Jenny L SonesPennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana; jsones@lsu.edu.
Cornell University · USLouisiana State University · USPennington Biomedical Research Center · US

Funding

Role of FGF21 in Protein Leverage and Placenta Function during PregnancyF31HD084199 · NICHD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI SUTTON, ELIZABETH FROST · 2016 to 2016
$34k
NICHD NIH HHS F31 HD084199
6 · The paper itself

Abstract

Preeclampsia (PE) is a devastating disorder of pregnancy that classically presents with maternal hypertension and proteinuria after 20 wk of gestation. In addition to being a leading cause of maternal and fetal morbidity/mortality, epidemiological and prospective studies have revealed long-term consequences for both the mother and baby of preeclamptic pregnancies, including chronic hypertension as well as other cardiovascular diseases and metabolic derangements. To better understand the effect of in utero exposure of PE on offspring, we utilized the BPH/5 mouse, a spontaneous model of the maternal and fetal PE syndrome. We hypothesized that young BPH/5 offspring would have altered metabolic and cardiovascular phenotypes. Indeed, BPH/5 growth-restricted offspring showed excess catch-up growth by early adulthood due to hyperphagia and increased white adipose tissue (WAT) accumulation, with inflammation markers isolated to the reproductive WAT depot only. Both excessive WAT accumulation and the inflammatory WAT phenotype were corrected by pair-feeding young BPH/5 female mice. We also found that young BPH/5 female mice showed evidence of leptin resistance. Indeed, chronic hyperleptinemia has been shown to characterize other rodent models of PE; however, the maternal metabolic profile before pregnancy has not been fully understood. Furthermore, we found that these mice show signs of cardiovascular anomalies (hypertension and cardiomegaly) and altered signaling within the reproductive axis in early life. Future studies will involve challenging the physiological metabolic state of BPH/5 mice through pair-feeding to reduce WAT before pregnancy and determining its causal role in adverse pregnancy outcomes.

Indexed as

Adipose Tissue, WhiteAnimalsAnimals, NewbornCardiovascular DiseasesFemaleHumansInfant, NewbornInfant, Newborn, DiseasesMetabolic DiseasesMiceMice, Inbred C57BLPre-EclampsiaPregnancyPrenatal Exposure Delayed EffectsBPH/5obesitypreeclampsiapregnancy

Identifiers

PMID28122721
PMCPMC5407079
OpenAlexW2581395626

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.