Esther Fuentes

TL;DR: 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.

TL;DR: It is shown here that xenoestrogens act at the genomic level by binding to intracellular estrogen receptors and trigger nongenomic effects in pancreatic beta cells, and an outline of the membrane receptor involved in rapidxenoestrogen actions is provided.

TL;DR: The purpose of the present review is to analyze with substantiated scientific evidence the strong estrogenic activity of BPA when it acts through alternative mechanisms of action at least in certain cell types.

TL;DR: It is shown that the endocrine disruptors bisphenol A (BPA) and diethylstilbestrol (DES) suppressed low-glucose–induced intracellular calcium ion ([Ca2+]i) oscillations in α-cells, the signal that triggers glucagon secretion.

TL;DR: Using quantitative real-time PCR and immunocytochemistry, it is demonstrated the existence of both CB1 and CB2 receptors in the endocrine pancreas and this effect may be a new component involved in the orexigenic effect of endocannabinoids and constitutes a potential target for pharmacologic manipulation of the energy balance.