Evidence map›Paper›PMID 25827101›Full record

ArticleArchives of toxicology2016

Programming of metabolic effects in C57BL/6JxFVB mice by in utero and lactational exposure to perfluorooctanoic acid.

J C J van Esterik, L Bastos Sales, M E T Dollé, H Håkansson, M Herlin, J Legler, L T M van der Ven

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In one paragraph

Article in Archives of toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Public health evaluation of PFAS exposures and breastfeeding: a systematic literature review.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Pooled it
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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

7 authors.

J C J van EsterikCenter for Health Protection, National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA, Bilthoven, The Netherlands.
L Bastos SalesDepartment of Chemistry and Biology, Institute for Environmental Studies (IVM), VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands.
M E T DolléCenter for Health Protection, National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA, Bilthoven, The Netherlands.
H HåkanssonInstitute of Environmental Medicine, Karolinska Institutet, P.O. Box 210, SE-171 77, Stockholm, Sweden.
M HerlinInstitute of Environmental Medicine, Karolinska Institutet, P.O. Box 210, SE-171 77, Stockholm, Sweden.
J LeglerDepartment of Chemistry and Biology, Institute for Environmental Studies (IVM), VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands.
L T M van der VenCenter for Health Protection, National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA, Bilthoven, The Netherlands. Leo.van.der.ven@RIVM.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perfluorooctanoic acid (PFOA) is known to cause developmental toxicity and is a suggested endocrine disrupting compound (EDC). Early life exposure to EDCs has been implicated in programming of the developing organism for chronic diseases later in life. Here we study perinatal metabolic programming by PFOA using an experimental design relevant for human exposure. C57BL/6JxFVB hybrid mice were exposed during gestation and lactation via maternal feed to seven low doses of PFOA at and below the NOAEL used for current risk assessment (3-3000 µg/kg body weight/day). After weaning, offspring were followed for 23-25 weeks without further exposure. Offspring showed a dose-dependent decrease in body weight from postnatal day 4 to adulthood. Growth under high fat diet in the last 4-6 weeks of follow-up was increased in male and decreased in female offspring. Both sexes showed increased liver weights, hepatic foci of cellular alterations and nuclear dysmorphology. In females, reductions in perigonadal and perirenal fat pad weights, serum triglycerides and cholesterol were also observed. Endocrine parameters, such as glucose tolerance, serum insulin and leptin, were not affected. In conclusion, our study with perinatal exposure to PFOA in mice produced metabolic effects in adult offspring. This is most likely due to disrupted programming of metabolic homeostasis, but the assayed endpoints did not provide a mechanistic explanation. The BMDL of the programming effects in our study is below the current point of departure used for calculation of the tolerable daily intake.

Indexed as

LactationPrenatal Exposure Delayed EffectsAnimalsBody WeightCaprylatesCholesterolDiet, High-FatDose-Response Relationship, DrugFemaleFluorocarbonsMaleMaternal ExposureMice, Inbred C57BLMice, Inbred StrainsOrgan SizePregnancyCaprylatesCholesterolFluorocarbonsperfluorooctanoic acidDevelopmental exposureEndocrine disrupting compoundsMetabolic effectsPerfluorooctanoic acidProgramming

Identifiers

PMID25827101
PMCPMC4754331

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Registered trials

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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.