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Int J Environ Res Public Health. 2019 Aug 28;16(17). pii: E3134. doi: 10.3390/ijerph16173134.

Chemical Effect of Bisphenol A on Non-Alcoholic Fatty Liver Disease.

Author information

1
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", via Pansini 5, 80131 Naples, Italy. marcello.dallio@gmail.com.
2
Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", via Pansini 5, 80131 Naples, Italy.
3
Department of Medicine and Surgery, University of Salerno, via Salvador Allende, 84081 Salerno, Italy.
4
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", via Pansini 5, 80131 Naples, Italy.
5
Department of Health Sciences, University "Magna Graecia", Viale Europa-Germaneto, 88110 Catanzaro, Italy.
6
Division of Gastroenterology, Department of Internal Medicine, TARGID, University Hospital Gasthuisberg, 3000 Leuven, Belgium.
7
Greenwood Genetic Center, 113 Gregor Mendel Circle, Greenwood, SC 29646, USA.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is considered a predominant chronic liver disease worldwide and a component of metabolic syndrome. Due to its relationship with multiple organs, it is extremely complex to precisely define its pathogenesis as well as to set appropriate therapeutic and preventive strategies. Endocrine disruptors (EDCs) in general, and bisphenol A (BPA) in particular, are a heterogeneous group of substances, largely distributed in daily use items, able to interfere with the normal signaling of several hormones that seem to be related to type 2 diabetes mellitus (T2DM), obesity, and other metabolic disorders. It is reasonable to hypothesize a BPA involvement in the pathogenesis and evolution of NAFLD. However, its mechanisms of action as well as its burden in the vicious circle that connects obesity, T2DM, metabolic syndrome, and NAFLD still remain to be completely defined. In this review we analyzed the scientific evidence on this promising research area, in order to provide an overview of the harmful effects linked to the exposure to EDCs as well as to frame the role that BPA would have in all phases of NAFLD evolution.

KEYWORDS:

bisphenol A; endocrine-disrupting compounds; hepatocellular carcinoma; non-alcoholic fatty liver disease; oxidative stress

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