Abstract
Bisphenol S (BPS) is a common replacement for bisphenol A (BPA) in plastics, which has resulted in widespread human exposure. Type 1 diabetes (T1D) is an autoimmune disease resulting from pancreatic β-cell destruction and has been increasing in incidence globally. Because of the similarities (e.g., endocrine disrupting) between BPS and BPA, and the fact that BPA was previously shown to accelerate T1D development in female non-obese diabetic (NOD) mice, it was hypothesized that BPS could contribute to the increasing T1D incidence by altering immunity with sex-biased responses. Adult female non-obese diabetic (NOD) mice were orally administered BPS at environmentally relevant doses (3, 30, 150 and 300 μg/kg), and males were given 0 or 300 μg/kg BPS. Females following 30 μg/kg BPS treatment on a soy-based diet had significantly delayed T1D development at the end of the study and decreased non-fasting blood glucose levels (BGLs) during the study. In contrast, BPS-exposed males on a soy-based diet showed an increased insulin resistance and varied BGLs. This might be a mixture effect with phytoestrogens, since males on a phytoestrogen-free diet showed improved glucose tolerance and decreased insulin resistance and CD25+ T cells. Additionally, while BPS altered BGLs in soy-based diet mice, minimal effects were observed concerning their immunotoxicity. Thus, BPS had sex- and diet-dependent effects on T1D and glucose homeostasis, which were likely caused by other mechanisms in addition to immunomodulation.
Highlights
Bisphenol S (BPS) is replacing bisphenol A (BPA), an established endocrine disrupting chemical (ED) used in a wide variety of polycarbonate plastics and epoxy resins
Modulation of diabetes by EDs might depend on diet as we have previously found diet-dependent effects from exposure to genistein, an ED, on type 1 diabetes (T1D) in streptozotocin-induced diabetic B6C3F1 male mice and from perinatal BPA exposure on T1D development in non-obese diabetic (NOD) mice [11,13]
To determine the effect of BPS on T1D, female NOD mice were exposed to BPS at doses of 0, 3, 30, 150 or 300 μg/kg during adulthood
Summary
Bisphenol S (BPS) is replacing bisphenol A (BPA), an established endocrine disrupting chemical (ED) used in a wide variety of polycarbonate plastics and epoxy resins. This has resulted in widespread exposure to BPS with its continuous buildup in the environment and use in plastic production [1,2]. BPA has previously been shown by us and others to dysregulate adult glucose homeostasis in humans [7] and accelerate T1D development and/or autoimmune responses in female non-obese diabetic (NOD) mice exposed during adulthood or the juvenile period [8,9,10,11] as well as streptozotocin-treated C57BL/6 male mice [12].
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