The Abstract from PlosOne

Bisphenol-A (BPA) is a widespread endocrine-disrupting chemical (EDC) used as the base compound in the manufacture of polycarbonate plastics. It alters pancreatic β-cell function and can be considered a risk factor for type 2 diabetes in rodents. Here we used ERβ−/− mice to study whether ERβ is involved in the rapid regulation of KATP channel activity, calcium signals and insulin release elicited by environmentally relevant doses of BPA (1 nM). We also investigated these effects of BPA in β-cells and whole islets of Langerhans from humans. 1 nM BPA rapidly decreased KATP channel activity, increased glucose-induced [Ca2+]i signals and insulin release in β-cells from WT mice but not in cells from ERβ−/− mice. The rapid reduction in the KATP channel activity and the insulinotropic effect was seen in human cells and islets. BPA actions were stronger in human islets compared to mouse islets when the same BPA concentration was used. Our findings suggest that BPA behaves as a strong estrogen via nuclear ERβ and indicate that results obtained with BPA in mouse β-cells may be extrapolated to humans. This supports that BPA should be considered as a risk factor for metabolic disorders in humans.

Two quick things

One: metabolism is, well, complex. The hunger regulating mechanism is for obvious reasons extremely primal and the system is shot through multiple redundancies and fail safes to ensure the organism does not accidently starve to death. As such you don’t want to hang your hat on such a minor result.

Two: At the same time. BPA looks exactly like what we would expect the obesity molecule to look it from a macro point of view. Its something that was suddenly everywhere. It works on a key channel. Even without any direct empirical evidence it would a plausible candidate for “metabolic lead.”

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