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Oestrogen receptor β mediates the actions of bisphenol-A on ion channel expression in mouse pancreatic beta cells – published online 27/06/2019

Fig from Martinez-Pinna paper

Juan Martinez-Pinna, Laura Marroqui, Abdelkrim Hmadcha, Javier Lopez-Beas, Sergi Soriano, Sabrina Villar-Pazos, Paloma Alonso-Magdalena, Reinaldo S. Dos Santos, Ivan Quesada, Franz Martin, Bernat Soria, Jan-Åke Gustafsson, Angel Nadal

Bisphenol-A (BPA) is an endocrine-disrupting chemical (EDC) found in many widely used products. BPA was detected in the urine of 93% of US citizens and its concentration in serum reaches between 1 and 25 nmol/l. Epidemiological studies have associated EDC exposure with type 2 diabetes in humans. BPA increases insulin levels and release in the presence of stimulatory glucose concentrations. In this issue, Martinez-Pinna, Marroqui et al (https://doi.org/10.1007/s00125-019-4925-y) report that BPA, at environmentally relevant doses, modulates the expression of more than 50 genes encoding Na+ and K+ ion channel subunits in mouse beta cells. BPA treatment resulted in decreased Na+ and K+ currents in islets, as well as modifying glucose-induced electrical activity. Using beta cells from oestrogen receptor β (Erβ) knockout mice, the authors demonstrated that the BPA-induced effects in pancreatic islets were dependent on oestrogen receptor β. They suggest that these results help to explain how BPA regulates insulin content and release and shed light upon the mechanisms by which EDCs with oestrogenic activity exert their diabetogenic activity.

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