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Review
. 2019 Aug 28;16(17):3134.
doi: 10.3390/ijerph16173134.

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

Marcello Dallio  1 , Nadia Diano  2 , Mario Masarone  3 , Antonietta Gerarda Gravina  4 , Vittorio Patanè  4 , Mario Romeo  4 , Rosa Di Sarno  4 , Sonia Errico  2 , Carla Nicolucci  2 , Ludovico Abenavoli  5 , Emidio Scarpellini  6 , Luigi Boccuto  7 , Marcello Persico  3 , Carmelina Loguercio  4 , Alessandro Federico  4
Affiliations
Review

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

Marcello Dallio et al. Int J Environ Res Public Health. .

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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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Main clinical bisphenol A (BPA) exposure-associated diseases.
Figure 2
Figure 2
BPA-mediated G protein-coupled receptor 30 (GPR30) activation and relative effects.
Figure 3
Figure 3
BPA-induced oxidative stress mechanisms.
See this image and copyright information in PMC

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