The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance

@article{AlonsoMagdalena2006TheEE,
  title={The Estrogenic Effect of Bisphenol A Disrupts Pancreatic $\beta$-Cell Function In Vivo and Induces Insulin Resistance},
  author={Paloma Alonso-Magdalena and Sumiko Morimoto and Cristina Ripoll and Esther Fuentes and Angel Nadal},
  journal={Environmental Health Perspectives},
  year={2006},
  volume={114},
  pages={106 - 112}
}
The function of the pancreatic β-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 17β-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 μg/kg) of either E2 or BPA induces a rapid decrease in glycemia that correlates with a rise of plasma… 

Figures from this paper

Effect of Bisphenol A on Insulin-Mediated Glucose Metabolism In Vivo and In Vitro

Exposure to BPA can induce insulin resistance by decreasing IR gene expression, which is followed by a decrease in insulin-mediated Akt activation and increased PTP1B activity.

Effect of bisphenol-A on insulin signal transduction and glucose oxidation in skeletal muscle of adult male albino rat

BPA has adverse effects on phosphorylation of Akt, GLUT4 translocation and 14C-glucose oxidation in skeletal muscle of male rat and increases pancreatic insulin content and favors postprandial hyperinsulinemia and insulin resistance in male mice.

Bisphenol A impairs insulin signaling and glucose homeostasis and decreases steroidogenesis in rat testis: an in vivo and in silico study.

Bisphenol A Induces Oxidative Stress and Decreases Levels of Insulin Receptor Substrate 2 and Glucose Transporter 8 in Rat Testis

The results suggest that persistent exposure to low doses of BPA could disturb glucose homeostasis in the testis and thereby impair testicular functions.

Short-Term Treatment with Bisphenol-A Leads to Metabolic Abnormalities in Adult Male Mice

The notion that BPA can be considered a risk factor for the development of type 2 diabetes is supported, as short-term treatment with low doses of BPA slows down whole body energy metabolism and disrupts insulin signaling in peripheral tissues.

Oestrogen receptor β mediates the actions of bisphenol-A on ion channel expression in mouse pancreatic beta cells

The data suggest that BPA modulates the expression and function of Na+ and K+ channels via ERβ in mouse pancreatic islets, and BPA alters beta cell electrical activity.

Rapid Insulinotropic Action of Low Doses of Bisphenol-A on Mouse and Human Islets of Langerhans: Role of Estrogen Receptor β

BPA behaves as a strong estrogen via nuclear ERβ and results obtained with BPA in mouse β-cells may be extrapolated to humans, suggesting that BPA should be considered as a risk factor for metabolic disorders in humans.
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