Prenatal exposure to perfluoroalkyl substances modulates neonatal serum phospholipids, increasing risk of type 1 diabetes

Aidan J. McGlinchey; Tim Sinioja; Santosh Lamichhane; Partho Sen; Johanna Bodin; Heli Siljander; Alex M. Dickens; Dawei Geng; Cecilia Carlsson; Daniel Duberg; Jorma Ilonen; Suvi Mirjami Virtanen; Hubert A. A. M. Dirven; Hanne Friis Berntsen; Karin Elisabeth Zimmer; Unni Cecilie Nygaard; Matej Orešič; Mikael Knip; Tuulia Hyötyläinen

doi:10.1016/j.envint.2020.105935

Molecular BiologyEnvironment InternationalJul 4, 2020

Peer-reviewed journal article

Prenatal exposure to perfluoroalkyl substances modulates neonatal serum phospholipids, increasing risk of type 1 diabetes

Aidan J. McGlinchey iD, Tim Sinioja iD, Santosh Lamichhane iD, Partho Sen iD, Johanna Bodin iD, Heli Siljander iD, Alex M. Dickens iD, Dawei Geng iD, Cecilia Carlsson, Daniel Duberg iD, Jorma Ilonen iD, Suvi Mirjami Virtanen iD, Hubert A. A. M. Dirven iD, Hanne Friis Berntsen iD, Karin Elisabeth Zimmer, Unni Cecilie Nygaard iD, Matej Orešič iD, Mikael Knip iD, Tuulia Hyötyläinen iD

Abstract

In the last decade, increasing incidence of type 1 diabetes (T1D) stabilized in Finland, a phenomenon that coincides with tighter regulation of perfluoroalkyl substances (PFAS). Here, we quantified PFAS to examine their effects, during pregnancy, on lipid and immune-related markers of T1D risk in children. In a mother-infant cohort (264 dyads), high PFAS exposure during pregnancy associated with decreased cord serum phospholipids and progression to T1D-associated islet autoantibodies in the offspring. This PFAS-lipid association appears exacerbated by increased human leukocyte antigen-conferred risk of T1D in infants. Exposure to a single PFAS compound or a mixture of organic pollutants in non-obese diabetic mice resulted in a lipid profile characterized by a similar decrease in phospholipids, a marked increase of lithocholic acid, and accelerated insulitis. Our findings suggest that PFAS exposure during pregnancy contributes to risk and pathogenesis of T1D in offspring.

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