Evidence map›Paper›PMID 36868448›Full record

ArticleEnvironmental research2023

Gene-environment interactions in the associations of PFAS exposure with insulin sensitivity and beta-cell function in a Faroese cohort followed from birth to adulthood.

Damaskini Valvi, David C Christiani, Brent Coull, Kurt Højlund, Flemming Nielsen, Karine Audouze, Li Su, Pal Weihe, Philippe Grandjean

Open access · greenAbstract read
In one paragraph

Article in Environmental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
11.6field-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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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

9 authors at 5 institutions in 4 countries.

Damaskini ValviDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States. Electronic address: dania.valvi@mssm.edu.
David C ChristianiDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States.
Brent CoullDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Kurt HøjlundSteno Diabetes Center Odense, Odense University Hospital, Odense, Denmark.
Flemming NielsenDepartment of Public Health, Clinical Pharmacology, Pharmacy and Environmental Medicine, University of Southern Denmark, Odense, Denmark.
Karine AudouzeUniversité Paris Cité, INSERM UMR-S1124, Paris, France.
Li SuDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States.
Pal WeiheDepartment of Occupational Medicine and Public Health, The Faroese Hospital System, Tórshavn, Faroe Islands; Centre of Health Science, Faculty of Health Sciences, University of the Faroe Islands, Tórshavn, Faroe Islands.
Philippe GrandjeanDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Department of Public Health, Clinical Pharmacology, Pharmacy and Environmental Medicine, University of Southern Denmark, Odense, Denmark.
Harvard University · USInserm · FRSteno Diabetes Centers · DKUniversity of Southern Denmark · DKUniversity of the Faroe Islands · FO

Funding

The Mount Sinai Transdisciplinary Center on Early Environmental ExposuresP30ES023515 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Manish Arora · 2014 to 2026
$21.3M
Sources, Transport, Exposure & Effects of PFAS (STEEP) Center - RENEWALP42ES027706 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI Elsie Mareca Sunderland · 2017 to 2026
$18.9M
Glucose Metabolism in Adults Prenatally Exposed to Diabetogenic PollutantsR01ES021477 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI GRANDJEAN, PHILIPPE ADAM · 2013 to 2017
$3.0M
Perfluoroalkyl substances and non-alcoholic fatty liver disease in children: Leveraging magnetic resonance imaging to unravel potential mechanisms and exposure mixture effectsR21ES035148 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI OULHOTE, YOUSSEF, VALVI, DAMASKINI · 2023 to 2023
$479k
Developmental Exposure to Perfluoroalkyl Substances and Cardiometabolic Outcomes in Adulthood: Potential Links via the Plasma MetabolomeR21ES029328 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI VALVI, DAMASKINI · 2019 to 2020
$425k
NIEHS NIH HHS P30 ES023515NIEHS NIH HHS P42 ES027706NIEHS NIH HHS R01 ES021477NIEHS NIH HHS R21 ES029328NIEHS NIH HHS R21 ES035148
6 · The paper itself

Abstract

backgroundExposure to perfluoroalkyl substances (PFAS) has been associated with changes in insulin sensitivity and pancreatic beta-cell function in humans. Genetic predisposition to diabetes may modify these associations; however, this hypothesis has not been yet studied.

objectivesTo evaluate genetic heterogeneity as a modifier in the PFAS association with insulin sensitivity and pancreatic beta-cell function, using a targeted gene-environment (GxE) approach.

methodsWe studied 85 single-nucleotide polymorphisms (SNPs) associated with type 2 diabetes, in 665 Faroese adults born in 1986-1987. Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were measured in cord whole blood at birth and in participants' serum from age 28 years. We calculated the Matsuda-insulin sensitivity index (ISI) and the insulinogenic index (IGI) based on a 2 h-oral glucose tolerance test performed at age 28. Effect modification was evaluated in linear regression models adjusted for cross-product terms (PFAS*SNP) and important covariates.

resultsPrenatal and adult PFOS exposures were significantly associated with decreased insulin sensitivity and increased beta-cell function. PFOA associations were in the same direction but attenuated compared to PFOS. A total of 58 SNPs were associated with at least one PFAS exposure variable and/or Matsuda-ISI or IGI in the Faroese population and were subsequently tested as modifiers in the PFAS-clinical outcome associations. Eighteen SNPs showed interaction p-values (P DISCUSSION: Findings from this study suggest that PFAS-associated changes in insulin sensitivity could vary between individuals as a result of genetic predisposition and warrant replication in independent larger populations.

Indexed as

Alkanesulfonic AcidsDiabetes Mellitus, Type 2Environmental PollutantsFluorocarbonsInsulin ResistanceAdultAlpha-Ketoglutarate-Dependent Dioxygenase FTOCaprylatesFemaleGene-Environment InteractionGenetic Predisposition to DiseaseHumansInfant, NewbornInsulinPregnancySolute Carrier Family 12, Member 3Alkanesulfonic AcidsAlpha-Ketoglutarate-Dependent Dioxygenase FTOCaprylatesEnvironmental PollutantsFluorocarbonsFTO protein, humanInsulinperfluorooctane sulfonic acidperfluorooctanoic acidSLC12A3 protein, humanSolute Carrier Family 12, Member 3DiabetesGene-environment interactionsPerfluoroalkyl substances

Identifiers

PMID36868448
PMCPMC10101920
OpenAlexW4322744559

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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.