Evidence map›Paper›PMID 33031959›Full record

ArticleMolecular metabolism2020

Ozone-induced fetal growth restriction in rats is associated with sexually dimorphic placental and fetal metabolic adaptation.

Colette N Miller, Janice A Dye, Andres R Henriquez, Erica J Stewart, Katelyn S Lavrich, Gleta K Carswell, Hongzu Ren, Danielle L Freeborn, Samantha J Snow, Mette C Schladweiler and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

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  7. Prenatal ozone exposure programs a sexually dimorphic susceptibility to high-fat diet in adolescent Long Evans rats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

15 authors at 2 institutions in 2 countries.

Colette N MillerPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA; Oak Ridge Institute for Science and Education Research Participation Program, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA. Electronic address: miller.colette@epa.gov.
Janice A DyePublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Andres R HenriquezOak Ridge Institute for Science and Education Research Participation Program, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Erica J StewartOak Ridge Institute for Science and Education Research Participation Program, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Katelyn S LavrichDivision of the National Toxicology Program, National Institute of Environmental Health Sciences, 530 Davis Dr., Keystone Building, Durham, NC, 27713, USA.
Gleta K CarswellBiomolecular and Computational Toxicology Division, Center for Computational Toxicology and Exposure, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Hongzu RenPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Danielle L FreebornPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Samantha J SnowPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Mette C SchladweilerPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Judy H RichardsPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Prasada R S KodavantiPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Anna FisherPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Brian N ChorleyBiomolecular and Computational Toxicology Division, Center for Computational Toxicology and Exposure, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Urmila P KodavantiPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Dr., Mail Code: B105-02, Research Triangle Park, NC, 27711, USA.
Environmental Protection Agency · USNational Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe importance of the placenta in mediating the pre- and post-natal consequences of fetal growth restriction has been increasingly recognized. However, the influence of placental sexual dimorphism on driving these outcomes has received little attention. The purpose of this study was to characterize how sex contributes to the relationship between placental metabolism and fetal programming utilizing a novel rodent model of growth restriction.

methodsFetal growth restriction was induced by maternal inhalation of 0.8 ppm ozone (4 h/day) during implantation receptivity (gestation days [GDs] 5 and 6) in Long-Evans rats. Control rats were exposed to filtered air. At GD 21, placental and fetal tissues were obtained for metabolic and genomic assessments.

resultsGrowth-restricted male placentae exhibited increased mitochondrial biogenesis, increased oxygen consumption, and reduced nutrient storage. Male growth-restricted fetuses also had evidence of reduced adiposity and downregulation of hepatic metabolic signaling. In contrast, placentae from growth-restricted females had elevated markers of autophagy accompanied by an observed protection against hepatic metabolic perturbations. Despite this, growth restriction in females induced a greater number of hypothalamic gene and pathway alterations compared to growth-restricted males.

conclusionsIncreases in mitochondrial metabolism in growth-restricted male placentae likely initiates a sequela of adaptations that promote poor nutrient availability and adiposity. Divergently, the female placenta expresses protective mechanisms that may serve to increase nutrient availability to support fetal metabolic development. Collectively, this work emphasizes the importance of sex in mediating alterations in placental metabolism and fetal programming.

Indexed as

AdiposityAnimalsFemaleFetal DevelopmentFetal Growth RetardationFetusMaleMitochondriaOzonePlacentaPregnancyPrenatal Exposure Delayed EffectsRatsRats, Long-EvansSex CharacteristicsSex FactorsOzoneDevelopmental origins of health and diseaseGrowth restrictionOzonePlacentaSex differences

Identifiers

PMID33031959
PMCPMC7588867
OpenAlexW3091848660

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.