The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance.

The function of the pancreatic beta-cell is the storage and release of insulin, the main hormone involved in blood glucose homeostasis. The results in this article show that the widespread environmental contaminant bisphenol-A (BPA) imitates 17beta-estradiol (E2) effects in vivo on blood glucose hom...

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Publicado en:Environmental Health Perspectives Vol. 114; no. 1; pp. 106 - 113
Autores principales: Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A
Formato: research tables/charts Journal Article
Publicado: National Institute of Environmental Health Sciences Jan2006
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jan2006
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        atl: The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance.
      aug:
        au:
          Alonso-Magdalena P
          Morimoto S
          Ripoll C
          Fuentes E
          Nadal A
        affil: Instituto de Bioingeniería, Universidad Miguel Hernández de Elche, Alicante, Spain.
      sug:
        subj:
          Estrogens
          Insulin Resistance
          Islets of Langerhans Drug Effects
          Phenols
          Animals
          Blood Glucose Analysis
          Funding Source
          Glucose Tolerance Test
          Insulin Blood
          Islets of Langerhans Metabolism
          Male
          Mice
          T-Tests
          Animal Studies
          Male
      ab: The function of the pancreatic beta-cell is the storage and release of insulin, the main hormone involved in blood glucose homeostasis. The results in this article show that the widespread environmental contaminant bisphenol-A (BPA) imitates 17beta-estradiol (E2) effects in vivo on blood glucose homeostasis through genomic and nongenomic pathways. The exposure of adult mice to a single low dose (10 microg/kg) of either E2 or BPA induces a rapid decrease in glycemia that correlates with a rise of plasma insulin. Longer exposures to E2 and BPA induce an increase in pancreatic beta-cell insulin content in an estrogen-receptor-dependent manner. This effect is visible after 2 days of treatment and starting at doses as low as 10 microg/kg/day. After 4 days of treatment with either E2 or BPA, these mice developed chronic hyperinsulinemia, and their glucose and insulin tolerance tests were altered. These experiments unveil the link between environmental estrogens and insulin resistance. Therefore, either abnormal levels of endogenous estrogens or environmental estrogen exposure enhances the risk of developing type 2 diabetes mellitus, hypertension, and dyslipidemia.
      pubtype: Academic Journal
      doctype:
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      ougenre: Article
    language: English
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