ArticleToxicology reports2016
Exposure to perfluoroundecanoic acid (PFUnDA) accelerates insulitis development in a mouse model of type 1 diabetes.
Article in Toxicology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Exposure to per- and polyfluoroalkyl substances (PFAS) and development of autoimmunity in humans and animals: a scoping review.Archives of toxicology · 2026Article
- PFOS and PFOA exposure induces liver injury and sex-dependent immune effects in C57BL/6 mice.iScience · 2026Article
- Article
- Revisiting type 1 diabetes progression in the non-obese diabetic mouse.Scientific reports · 2026Article
- Effect of Per and Poly-Fluoroalkyl Substances on Pregnancy and Child Development.Current pediatric reviews · 2025Review
- Per- and polyfluoroalkyl substances alter innate immune function: evidence and data gaps.Journal of immunotoxicology · 2024Review
- Exploring Toxicity of Per- and Polyfluoroalkyl Substances (PFAS) Mixture Through ADMET and Toxicogenomic In Silico Analysis: Molecular Insights.International journal of molecular sciences · 2024Article
- PFAS Exposures and the Human Metabolome: A Systematic Review of Epidemiological Studies.Current pollution reports · 2023Article
- Environmental Exposure to Emerging Alternatives of Per- and Polyfluoroalkyl Substances and Polycystic Ovarian Syndrome in Women Diagnosed with Infertility: A Mixture Analysis.Environmental health perspectives · 2023Article
- PFAS release from wastewater residuals as a function of composition and production practices.Environmental pollution (Barking, Essex : 1987) · 2023Article
- Critical Overview on Endocrine Disruptors in Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Consideration of pathways for immunotoxicity of per- and polyfluoroalkyl substances (PFAS).Environmental health : a global access science source · 2023Review
- Exposure to persistent organic pollutants alters the serum metabolome in non-obese diabetic mice.Metabolomics : Official journal of the Metabolomic Society · 2022Article
- The effect of spermidine on autoimmunity and beta cell function in NOD mice.Scientific reports · 2022Article
- Associations between Exposures to Perfluoroalkyl Substances and Diabetes, Hyperglycemia, or Insulin Resistance: A Scoping Review.Journal of xenobiotics · 2021Article
- Per- and Polyfluoroalkyl Substance Toxicity and Human Health Review: Current State of Knowledge and Strategies for Informing Future Research.Environmental toxicology and chemistry · 2021Review
- Lipidomic Analyses Reveal Modulation of Lipid Metabolism by the PFAS Perfluoroundecanoic Acid (PFUnDA) in Non-Obese Diabetic Mice.Frontiers in genetics · 2021Article
- Perfluoroalkyl substances and cognitive function in older adults: Should we consider non-monotonic dose-responses and chronic kidney disease?Environmental research · 2021Article
- Metabolic Signatures of the Exposome-Quantifying the Impact of Exposure to Environmental Chemicals on Human Health.Metabolites · 2020Review
- Endocrine Disrupting Chemicals and Type 1 Diabetes.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perfluoralkylated substances (PFAS) are classified as persistent, bioaccumulative and toxic substances and are widespread environmental contaminants. Humans are exposed through food, drinking water and air. We have previously reported that bisphenol A accelerates spontaneous diabetes development in non-obese diabetic (NOD) mice and observed in the present study that perfluoroundecanoic acid, PFUnDA, increased insulitis development, a prerequisite for diabetes development in NOD mice. We exposed NOD mice to PFUnDA in drinking water (3, 30 and 300 μg/l) at mating, during gestation and lactation and until 30 weeks of age. After 300 μg/l PFUnDA exposure, we report (i) increased pancreatic insulitis, (ii) increased number of apoptotic cells in pancreatic islets prior to insulitis and (iii) decreased phagocytosis in peritoneal macrophages. There was also a trend of decreased number of tissue resident macrophages in pancreatic islets prior to insulitis after exposure to 300 μg/l, and altered cytokine secretion in activated splenocytes after exposure to 3 μg/l PFUnDA. Although insulitis is a prerequisite for autoimmune diabetes, the accelerated insulitis was not associated with accelerated diabetes development. Instead, the incidence of diabetes tended to be reduced in the animals exposed to 3 and 30 μg/l PFUnDA, suggesting a non-monotonic dose response. The effects of PFUnDA exposure on increased apoptosis in pancreas and reduced macrophage function as well as accelerated insulitis development in NOD mice, may also be relevant for human insulitis. Further observational autoimmune diabetes clinical cohort studies and animal experiments for PFUnDA as well as other PFASs are therefore encouraged.
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