Are BPA Substitutes as Obesogenic as BPA?

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.

Bisphenol A is a carcinogen that induces lipid accumulation, peroxisome proliferator‑activated receptor‑γ expression and liver disease

“…BPA exhibits obesogenic properties that alter PPARγ mRNA expression in THLE-2 cells. The obesogenic properties include adipogenesis, stimulating lipid accumulation in adipose tissue and liver, and perturbs obesity-related cytokines levels (40,41). The expression of this adipogenesis gene or lipid sensor indicates an increase in lipid accumulation and adipogenesis in the liver in response to BPA exposure.…”

Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus

“…Herein, we focus on the effects of BPs on glucose homeostasis and pancreatic β-cell function and viability. Recent reviews have addressed diabetes, obesity, and nonalcoholic fatty liver disease ( 5 , 27 , 53 , 54 ).…”

Exposure to Bisphenol A Substitutes, Bisphenol S and Bisphenol F, and Its Association with Developing Obesity and Diabetes Mellitus: A Narrative Review

“…In several in vivo and in vitro studies, BPA exposure was shown to promote significant disturbances in glucose homeostasis and insulin sensitivity. Impairments in lipid metabolism and the promotion of fat accumulation were also observed [ 9 , 10 , 11 ]. In addition, epidemiological studies have reported that urinary and/or serum BPA concentrations are strongly associated with an increased incidence of obesity [ 12 , 13 , 14 ] and diabetes [ 15 , 16 , 17 , 18 ].…”

“…Indeed, BPS and BPF are structurally and chemically similar to BPA ( Figure 1 ); thus, they are expected to promote adverse effects by acting as endocrine disrupters [ 11 ]. Recently, BPS and BPF were reported to promote fat accumulation in adipocytes [ 27 , 28 ].…”