Sex- and Dose-Specific Effects of Maternal Bisphenol A Exposure on Pancreatic Islets.


Dr Swati Bhave    06 December 2017

Exposure to the environmental endocrine disruptor bisphenol A (BPA) is omnipresent and associated with the increased risk of diabetes and obesity.

A recent study published in Environmental Health Perspectives demonstrated that perinatal BPA exposure is associated with higher body fat, impaired glucose tolerance, and reduced insulin secretion. The purpose of this study was to determine the multigenerational effects of maternal bisphenol A exposure on mouse pancreatic islets.

In this experiment, cellular and molecular mechanisms underlying the persistent effects of maternal bisphenol A exposure were determined in F1 and F2 adult offspring of F0 mothers exposed to two relevant human exposure levels of BPA (10μg/kg/d-LowerB and 10mg/kg/d-UpperB).

It was found that both doses of BPA markedly impaired insulin secretion in male, but not in female F1 and F2 offspring. Remarkably, LowerB and UpperB induced islet inflammation in male F1 offspring that persisted into the next generation. In addition, in male offspring, UpperB exposure hindered mitochondrial function, whereas LowerB exposure significantly reduced beta-cell mass and increased beta-cell death that persisted in the F2 generation. Furthermore, there were notable dose-specific changes in the expression of genes regulating inflammation and mitochondrial function. It was reported that the increased expression of the critically important beta-cell gene, insulin-like growth factor 2 (IGF-2) in whole F1 embryos were previously observed. Here, results revealed that the increased IGF-2 expression persisted in the islets of male F1 and F2 offspring and was associated with altered DNA methylation.

From the findings, it was inferred that maternal BPA exposure has dose- and sex-specific effects on pancreatic islets of adult F1 and F2 mice offspring. It was stated that the transmission of these changes across multiple generations may involve either mitochondrial dysfunction and/or epigenetic modifications.

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