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BPA accelerates diabetes in NOD mice

Discussion in 'Research' started by sgh, Nov 6, 2013.

  1. sgh

    sgh Approved members

    Joined:
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    New study on a topic near and dear to me-- never been done before-- very exciting to see this. Maybe this will trigger some more research on the topic!
    I haven't gotten the full text yet but will do so shortly.

    Toxicol Sci. 2013 Nov 4. [Epub ahead of print]

    Transmaternal bisphenol A exposure accelerates diabetes type 1 development in NOD mice.

    Bodin J, Kocbach B?lling A, Becher R, Kuper F, Lovik M, Nygaard UC.

    Source
    Department of Food, Water and Cosmetics, Norwegian Institute of Public Health, Oslo, Norway.

    Abstract

    Diabetes mellitus type 1 (T1DM) is an autoimmune disease with a genetic predisposition that is triggered by environmental factors during early life. Epidemiological studies show that bisphenol A (BPA), an endocrine disruptor, has been detected in about 90% of all analysed human urine samples. In this study, BPA was found to increase the severity of insulitis and the incidence of diabetes in female non obese diabetic (NOD) mice offspring after transmaternal exposure through the dams' drinking water (0, 0.1, 1 and 10mg/l). Both the severity of insulitis in the pancreatic islets at 11 weeks of age and the diabetes prevalence at 20 weeks were significantly increased for female offspring in the highest exposure group compared to the control group. Increased numbers of apoptotic cells, a reduction in tissue resident macrophages and an increase in regulatory T cells were observed in islets prior to insulitis development in transmaternally exposed offspring. The detectable apoptotic cells were identified as mostly glucagon producing alpha-cells but also tissue resident macrophages and beta-cells. In the local (pancreatic) lymph node neither regulatory T cell nor NKT cell populations were affected by maternal BPA exposure. Maternal BPA exposure may have induced systemic immune changes in offspring, as evidenced by alterations in LPS- and ConA-induced cytokine secretion in splenocytes. In conclusion, transmaternal BPA exposure, in utero and through lactation, accelerated the spontaneous diabetes development in NOD mice. This acceleration appeared to be related to early life modulatory effects on the immune system, resulting in adverse effects later in life.

    http://www.ncbi.nlm.nih.gov/pubmed/24189131

    ~Sarah Howard
    www.diabetesandenvironment.org
     

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