Per- and polyfluoroalkyl substance plasma concentrations and metabolomic markers of type 2 diabetes in the Diabetes Prevention Program trial.


Journal

International journal of hygiene and environmental health
ISSN: 1618-131X
Titre abrégé: Int J Hyg Environ Health
Pays: Germany
ID NLM: 100898843

Informations de publication

Date de publication:
03 2021
Historique:
received: 10 09 2020
revised: 24 11 2020
accepted: 02 12 2020
pubmed: 22 12 2020
medline: 26 10 2021
entrez: 21 12 2020
Statut: ppublish

Résumé

Per- and polyfluoroalkyl substances (PFAS) are widely used chemicals, some of which have been linked to type 2 diabetes. We tested whether PFAS concentrations were cross-sectionally associated with metabolites previously shown to predict incident type 2 diabetes using the Diabetes Prevention Program (DPP), a trial of individuals at high risk of type 2 diabetes. We evaluated 691 participants enrolled in the DPP with baseline measures of 10 PFAS (including total perfluorooctanesulfonic acid (PFOS), total perfluorooctanoic acid (PFOA), and Sb-PFOA [branched isomers of PFOA]) and 77 metabolites. We used log Sb-PFOA was associated with the largest number of tested metabolites (29 of 77). Each doubling in Sb-PFOA was associated with higher leucine (β = 0.07 [95%CI: 0.02, 0.11] SD) and lower glycine (-0.08 [95%CI: 0.03, -0.13] SD). Each doubling of either total PFOA or n-PFOA was associated with -0.13 [95%CI: 0.04, -0.22] SD lower glycine. PFOA and Sb-PFOA were positively associated with multiple triacylglycerols and diacylglycerols, and total PFOS, total PFOA, and Sb-PFOA were positively associated with phosphatidylethanolamines. PFAS concentrations are associated with metabolites linked to type 2 diabetes (particularly amino acid, glycerolipid and glycerophospholipid pathways). Further prospective research is needed to test whether these metabolites mediate associations of PFAS and type 2 diabetes.

Sections du résumé

BACKGROUND
Per- and polyfluoroalkyl substances (PFAS) are widely used chemicals, some of which have been linked to type 2 diabetes. We tested whether PFAS concentrations were cross-sectionally associated with metabolites previously shown to predict incident type 2 diabetes using the Diabetes Prevention Program (DPP), a trial of individuals at high risk of type 2 diabetes.
METHODS
We evaluated 691 participants enrolled in the DPP with baseline measures of 10 PFAS (including total perfluorooctanesulfonic acid (PFOS), total perfluorooctanoic acid (PFOA), and Sb-PFOA [branched isomers of PFOA]) and 77 metabolites. We used log
RESULTS
Sb-PFOA was associated with the largest number of tested metabolites (29 of 77). Each doubling in Sb-PFOA was associated with higher leucine (β = 0.07 [95%CI: 0.02, 0.11] SD) and lower glycine (-0.08 [95%CI: 0.03, -0.13] SD). Each doubling of either total PFOA or n-PFOA was associated with -0.13 [95%CI: 0.04, -0.22] SD lower glycine. PFOA and Sb-PFOA were positively associated with multiple triacylglycerols and diacylglycerols, and total PFOS, total PFOA, and Sb-PFOA were positively associated with phosphatidylethanolamines.
CONCLUSIONS
PFAS concentrations are associated with metabolites linked to type 2 diabetes (particularly amino acid, glycerolipid and glycerophospholipid pathways). Further prospective research is needed to test whether these metabolites mediate associations of PFAS and type 2 diabetes.

Identifiants

pubmed: 33348273
pii: S1438-4639(20)30626-X
doi: 10.1016/j.ijheh.2020.113680
pmc: PMC8630734
mid: NIHMS1657005
pii:
doi:

Substances chimiques

Biomarkers 0
Environmental Pollutants 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

113680

Subventions

Organisme : NIDDK NIH HHS
ID : U01 DK048412
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048375
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048434
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048413
Pays : United States
Organisme : NIEHS NIH HHS
ID : K23 ES024803
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR002534
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048339
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048514
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048468
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048387
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048404
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES024765
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048489
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048437
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048407
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030101
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048397
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048381
Pays : United States
Organisme : NIEHS NIH HHS
ID : T32 ES007069
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048443
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048380
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK048400
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier GmbH. All rights reserved.

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Auteurs

Susanna D Mitro (SD)

Population Health Sciences Program, Harvard University, Boston, MA, USA.

Jinxi Liu (J)

Department of Epidemiology and Biostatistics, Biostatistics Center and Milken Institute School of Public Health, George Washington University, Rockville, MD, USA.

Lindsay M Jaacks (LM)

Department of Global Health and Population, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

Abby F Fleisch (AF)

Pediatric Endocrinology and Diabetes, Maine Medical Center and Center for Outcomes Research and Evaluation, Maine Medical Center Research Institute, Portland, ME, USA.

Paige L Williams (PL)

Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.

William C Knowler (WC)

National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, AZ, USA.

Blandine Laferrère (B)

New York Obesity Research Center, Division of Endocrinology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA.

Wei Perng (W)

Department of Epidemiology, Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, Colorado School of Public Health, University of Colorado Denver Anschutz Medical Campus, Aurora, CO, USA.

George A Bray (GA)

Pennington Biomedical Research Center/Louisiana State University, Baton Rouge, LA, USA.

Amisha Wallia (A)

Division of Endocrinology, Metabolism, and Molecular Medicine, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.

Marie-France Hivert (MF)

Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA; Diabetes Unit, Massachusetts General Hospital, Boston, MA, USA.

Emily Oken (E)

Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA.

Tamarra M James-Todd (TM)

Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Harvard T.H. Chan School of Public Health and Division of Women's Health, Department of Medicine, Connors Center for Women's Health and Gender Biology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Marinella Temprosa (M)

Department of Epidemiology and Biostatistics, Biostatistics Center and Milken Institute School of Public Health, George Washington University, Rockville, MD, USA. Electronic address: dppmail@bsc.gwu.edu.

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Classifications MeSH