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Review
. 2022 Apr 11;23(8):4238.
doi: 10.3390/ijms23084238.

Are BPA Substitutes as Obesogenic as BPA?

Fabiana Oliviero  1 , Alice Marmugi  1 , Catherine Viguié  1 , Véronique Gayrard  1 , Nicole Picard-Hagen  1 , Laila Mselli-Lakhal  1
Affiliations
Review

Are BPA Substitutes as Obesogenic as BPA?

Fabiana Oliviero et al. Int J Mol Sci. .

Abstract

Metabolic diseases, such as obesity, Type II diabetes and hepatic steatosis, are a significant public health concern affecting more than half a billion people worldwide. The prevalence of these diseases is constantly increasing in developed countries, affecting all age groups. The pathogenesis of metabolic diseases is complex and multifactorial. Inducer factors can either be genetic or linked to a sedentary lifestyle and/or consumption of high-fat and sugar diets. In 2002, a new concept of "environmental obesogens" emerged, suggesting that environmental chemicals could play an active role in the etiology of obesity. Bisphenol A (BPA), a xenoestrogen widely used in the plastic food packaging industry has been shown to affect many physiological functions and has been linked to reproductive, endocrine and metabolic disorders and cancer. Therefore, the widespread use of BPA during the last 30 years could have contributed to the increased incidence of metabolic diseases. BPA was banned in baby bottles in Canada in 2008 and in all food-oriented packaging in France from 1 January 2015. Since the BPA ban, substitutes with a similar structure and properties have been used by industrials even though their toxic potential is unknown. Bisphenol S has mainly replaced BPA in consumer products as reflected by the almost ubiquitous human exposure to this contaminant. This review focuses on the metabolic effects and targets of BPA and recent data, which suggest comparable effects of the structural analogs used as substitutes.

Keywords: BPA substitutes; endocrine disruptors; metabolic disorders.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Overview of BPA effects on energy metabolism.
Figure 2
Figure 2
Mode of action of BPA on pancreatic β-cells [37]. This figure reports the mode of action of BPA on pancreatic cells. Low concentrations of BPA interact with Erα, Erβ and GPR30 receptors. ERα is involved in the regulation of pancreatic insulin biosynthesis in response to BPA. Erβ participates in the insulinotropic effect of BPA on pancreatic β-cells by rapidly decreasing KATP channel activity, enhancing glucose-induced [Ca2+] signals and insulin release. GPR30 is a non-classical membrane estrogen receptor that may participate in the insulinotropic effect of BPA on pancreatic β-cells.
Figure 3
Figure 3
Illustration of non-monotone effects of BPA on genes involved in glucose and lipid metabolism in the liver according to Mamugi et al., 2012.
See this image and copyright information in PMC

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