SummarySeveral studies associate foetal human exposure to bisphenol A (BPA) tometabolic/endocrine diseases, mainly diabesity. They describe the role of BPA inthe disruption of pancreatic beta cell, adipocyte and hepatocyte functions. Indeed,the complexity of the diabesity phenotype is due to the involvement of differentendoderm-derived organs, all targets of BPA.Here, we analyse this point delineating a picture of different mechanisms of BPAtoxicity in endoderm-derived organs leading to diabesity. Moving from epidemiologicaldata, we summarize the in vivo experimental data of the BPA effects onendoderm-derived organs (thyroid, pancreas, liver, gut, prostate and lung) afterprenatal exposure. Mainly, we gather molecular data evidencing harmful effectsat low-dose exposure, pointing to the risk to human health. Although the fragmentationof molecular data does not allow a clear conclusion to be drawn, the presentwork indicates that the developmental exposure to BPA represents a risk forendoderm-derived organs development as it deregulates the gene expression fromthe earliest developmental stages.A more systematic analysis of BPA impact on the transcriptomes of endodermderivedorgans is still missing. Here, we suggest in vitro toxicogenomics approachesas a tool for the identification of common mechanisms of BPA toxicity leading tothe diabesity in organs having the same developmental origin.
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