Prenatal exposure to perfluoroalkyl substances modulates neonatal serum phospholipids, increasing risk of type 1 diabetes
By Aidan McGlinchey, Tim Sinioja, Santosh Lamichhane, Partho Sen, Johanna Bodin, Heli Siljander, Alex M Dickens, Dawei Geng, Cecilia Carlsson, Daniel Duberg, Jorma Ilonen, Suvi M Virtanen, Hubert Dirven, Hanne Friis Berntsen, Karin Zimmer, Unni C Nygaard, Matej Orešič, Mikael Knip, and Tuulia Hyötyläinen
July 13, 2020
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.