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Bodin J, Kocbach Bølling A, Wendt A, et al. Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice. Toxicol Rep. 2015;2:99-110doi: 10.1016/j.toxrep.2015.02.010.
Bodin, J., Kocbach Bølling, A., Wendt, A., Eliasson, L., Becher, R., Kuper, F., Løvik, M., & Nygaard, U. C. (2015). Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice. Toxicology reports, 299-110. https://doi.org/10.1016/j.toxrep.2015.02.010
Bodin, Johanna, et al. "Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice." Toxicology reports vol. 2 (2015): 99-110. doi: https://doi.org/10.1016/j.toxrep.2015.02.010
Bodin J, Kocbach Bølling A, Wendt A, Eliasson L, Becher R, Kuper F, Løvik M, Nygaard UC. Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice. Toxicol Rep. 2015 Feb 28;2:99-110. doi: 10.1016/j.toxrep.2015.02.010. eCollection 2015. PMID: 28962342; PMCID: PMC5598488.
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Toxicol Rep. 2015 Feb 28;2:99-110. doi: 10.1016/j.toxrep.2015.02.010. eCollection 2015.

Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice.

Toxicology reports

Johanna Bodin, Anette Kocbach Bølling, Anna Wendt, Lena Eliasson, Rune Becher, Frieke Kuper, Martinus Løvik, Unni Cecilie Nygaard

Affiliations

  1. Department of Food, Water and Cosmetics, Norwegian Institute of Public Health, Oslo, Norway.
  2. Department of Air Pollution and Noise, Norwegian Institute of Public Health, Oslo, Norway.
  3. Lund University Diabetes Centre, Department of Clinical Sciences Malmö, Islet Cell Exocytosis, Lund University, CRC, Malmö, Sweden.
  4. TNO, Zeist, The Netherlands.
  5. Department for Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University for Science and Technology, Trondheim, Norway.

PMID: 28962342 PMCID: PMC5598488 DOI: 10.1016/j.toxrep.2015.02.010

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune destruction of insulin producing pancreatic beta-cells due to a genetic predisposition and can be triggered by environmental factors. We have previously shown that bisphenol A (BPA) accelerates the spontaneous development of diabetes in non-obese diabetic (NOD) mice. Here, we hypothesized that oral exposure to a mixture of the endocrine disruptors BPA and phthalates, relevant for human exposure, would accelerate diabetes development compared to BPA alone. NOD mice were exposed to BPA (1 mg/l), a mixture of phthalates (DEHP 1 mg/l, DBP 0.2 mg/l, BBP 10 mg/l and DiBP 20 mg/l) or a combination of BPA and the phthalate mixture through drinking water from conception and throughout life. Previous observations that BPA exposure increased the prevalence of diabetes and insulitis and decreased the number of tissue resident macrophages in pancreas were confirmed, and extended by demonstrating that BPA exposure also impaired the phagocytic activity of peritoneal macrophages. None of these effects were observed after phthalate exposure alone. The phthalate exposure in combination with BPA seemed to dampen the BPA effects on macrophage number and function as well as diabetes development, but not insulitis development. Exposure to BPA alone or in combination with phthalates decreased cytokine release (TNFα, IL-6, IL-10, IFNγ, IL-4) from

Keywords: BBP, butylbenzyl phthalate; BPA, bisphenol A; Bisphenol A; DBP, dibutyl phthalate; DEHP, bis(2-ethylhexyl) benzene-1,2-dicarboxylate; DiBP, diisobutyl phthalate; Diabetes mellitus type 1; Immunotoxicity; Insulitis; NOD mice; Phthalates; Prenatal exposure

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