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Exposure to persistent organic pollutants alters the serum metabolome in non-obese diabetic mice

Orešič Matej; Nygaard Unni C.; Berntsen Hanne Friis; Dirven Hubert; Hyötyläinen Tuula; Bodin Johanna; Sinioja Tim; Zimmer Karin; Duberg Daniel

Exposure to persistent organic pollutants alters the serum metabolome in non-obese diabetic mice

Orešič Matej
Nygaard Unni C.
Berntsen Hanne Friis
Dirven Hubert
Hyötyläinen Tuula
Bodin Johanna
Sinioja Tim
Zimmer Karin
Duberg Daniel
Katso/Avaa
Exposure to persistent organic pollutants alters the serum metabolome in non-obese diabetic mice.pdf (1.439Mb)
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SPRINGER
doi:10.1007/s11306-022-01945-0
URI
http://dx.doi.org/10.1007%2Fs11306-022-01945-0
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2022112967648
Tiivistelmä

Introduction
Autoimmune disorders such as type 1 diabetes (T1D) are believed to be caused by the interplay between several genetic and environmental factors. Elucidation of the role of environmental factors in metabolic and immune dysfunction leading to autoimmune disease is not yet well characterized.

Objectives
Here we investigated the impact of exposure to a mixture of persistent organic pollutants (POPs) on the metabolome in non-obese diabetic (NOD) mice, an experimental model of T1D. The mixture contained organochlorides, organobromides, and per- and polyfluoroalkyl substances (PFAS).

Methods
Analysis of molecular lipids (lipidomics) and bile acids in serum samples was performed by UPLC-Q-TOF/MS, while polar metabolites were analyzed by GC-Q-TOF/MS.

Results
Experimental exposure to the POP mixture in these mice led to several metabolic changes, which were similar to those previously reported as associated with PFAS exposure, as well as risk of T1D in human studies. This included an increase in the levels of sugar derivatives, triacylglycerols and lithocholic acid, and a decrease in long chain fatty acids and several lipid classes, including phosphatidylcholines, lysophosphatidylcholines and sphingomyelins.

Conclusion
Taken together, our study demonstrates that exposure to POPs results in an altered metabolic signature previously associated with autoimmunity.

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