1 National Laboratory of Endocrine Disruptors, National Institute of Biostructures and Biosystems (INBB), Via P. Castellino, 111, 80131 Naples, Italy
2 Institute of Genetics and Biomedical Research – CNR UOS Milano c/o Humanitas Clinical Institute Research Center, Via Manzoni 113, 20089 Rozzano, Milano, Italy
3 Institute of Genetic and Biophysics – CNR, Via P. Castellino, 111, 80131 Naples, Italy
4 Department of Experimental Medicine, Second University of Naples, Via S.M. di Costantinopoli, 16, 80138 Naples, Italy
5 Departments of Obstetrics and Gynecology and Reproductive Sciences and Neurobiology, Section of Comparative Medicine and Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, 333 Cedar Street New Haven, CT 06520, USA
Bisphenol A (BPA) is used as basic chemical compound in the production of polycarbonate food containers or epoxy resins coating metallic cans for food and beverages conservation. Its xeno-estrogenic activity alters endocrine-metabolic pathways modulating glucose metabolism and increasing the risk of developing diabetes, insulin resistance, and obesity. Based on in vitro and in vivo experimental research, here we report some of the major BPA adverse effects on tissues that play a key role in the regulation on the whole body’s metabolism. Evidences have shown that BPA is able to exert its endocrine disrupting action altering glucose metabolism and contributing to the onset of metabolic disorders, acting on liver functions and affecting insulin production by the pancreas. Exposure to BPA has been reported also to modulate glucose utilization in muscles, as well as to interfere with adipose tissue endocrine function. In addition, to peripheral tissues, recent studies have shown that BPA by acting in the Central Nervous System affects neuroendocrine regulation of glucose metabolism, promoting glucose metabolism dysfunction such as glucose intolerance and insulin resistance. Thus, exposure to BPA seems to be an important risk factor in the onset of obesity and metabolic syndrome. However, its mechanisms of action need to be further investigated to provide a major evaluation of risk assessment.
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* Address correspondence to this author at the Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine at the Departments of Obstetrics, and Gynecology and Reproductive Sciences, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA; Tel: +1203 737 1216; Fax: +1203 785 4713;