Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis
Article first published online: 30 OCT 2007
DOI: 10.1111/j.1365-2605.2007.00832.x
© 2008 The Authors
Additional Information
How to Cite
Ropero, A. B., Alonso-Magdalena, P., García-García, E., Ripoll, C., Fuentes, E. and Nadal, A. (2008), Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis. International Journal of Andrology, 31: 194–200. doi: 10.1111/j.1365-2605.2007.00832.x
Publication History
- Issue published online: 30 OCT 2007
- Article first published online: 30 OCT 2007
- Received 2 July 2007; revised 7 September 2007; accepted 21 September 2007
- Abstract
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Keywords:
- diabetes;
- endocrine disruptors;
- oestrogen receptors;
- insulin resistance;
- metabolic syndrome
Summary
The link between endocrine disruptors and altered blood glucose homeostasis has been recently suggested. Epidemiological studies have correlated levels of phthalates, dioxins and persistent organic pollutants with alterations of blood glucose homeostasis in humans. Environmentally relevant doses of the ubiquitous endocrine disruptor bisphenol-A (BPA) have profound effects on mice endocrine pancreas – an essential tissue involved in glucose metabolism. BPA exerts rapid non-genomic effects on insulin releasing β-cells and glucagon releasing α-cells within freshly isolated islets of Langerhans. In vivo, a single BPA injection of 10μg/kg rapidly increases plasma insulin and concomitantly decreases glycaemia. When mice were treated with BPA 100μg/kg/day for 4 days, the environmental oestrogen produced an increase in β-cell insulin content along with a post-prandial hyperinsulinaemia and insulin resistance. The results reviewed here demonstrate that doses well below the current lowest observed adverse effect level considered by the US-EPA, disrupt pancreatic β-cell function producing insulin resistance in male mice. Therefore, this altered blood glucose homeostasis by BPA exposure may enhance the risk of developing type II diabetes.

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