Bisphenol A, obesity, and type 2 diabetes mellitus: genuine concern or unnecessary preoccupation?

Epidemiologic and experimental studies have associated changes of blood glucose homeostasis to Bisphenol A (BPA) exposure. We took a toxicogenomic approach to investigate the mechanisms of low-dose (1 × 10−9 M) BPA toxicity in ex vivo cultures of primary murine pancreatic islets and hepatocytes. Twenty-nine inhibited genes were identified in islets and none in exposed hepatocytes. Although their expression was slightly altered, their impaired cellular level, as a whole, resulted in specific phenotypic changes. Damage of mitochondrial function and metabolism, as predicted by bioinformatics analyses, was observed: BPA exposure led to a time-dependent decrease in mitochondrial membrane potential, to an increase of ROS cellular levels and, finally, to an induction of apoptosis, attributable to the bigger Bax/Bcl-2 ratio owing to activation of NF-κB pathway. Our data suggest a multifactorial mechanism for BPA toxicity in pancreatic islets with emphasis to mitochondria dysfunction and NF-κB activation. Finally, we assessed in vitro the viability of BPA-treated islets in stressing condition, as exposure to high glucose, evidencing a reduced ability of the exposed islets to respond to further damages. The result was confirmed in vivo evaluating the reduction of glycemia in hyperglycemic mice transplanted with control and BPA-treated pancreatic islets. The reported findings identify the pancreatic islet as the main target of BPA toxicity in impairing the glycemia. They suggest that the BPA exposure can weaken the response of the pancreatic islets to damages. The last observation could represent a broader concept whose consideration should lead to the development of experimental plans better reproducing the multiple exposure conditions.

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“…8, 9, 10, 11, 12 It is used in the manufacture of polycarbonates and epoxy resins. Its polymers, not toxic, are used in food contact materials.…”

mentioning

confidence: 99%

Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

et al. 2015

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“…Epidemiological studies Several recent reviews have been published concerning epidemiological data and the link between BPA exposure and obesity [39,[48][49][50][51].…”

Section: Impact Of Bpa In Obesitymentioning

confidence: 99%

Is bisphenol A an environmental obesogen?

Legeay

Faure

2017

Fundamemntal Clinical Pharma

104

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Bisphenol A (BPA) is an endocrine disruptor with an oestrogenic activity that is widely produced for the manufacture of polycarbonate plastic, epoxy resin, and thermal paper. Its ubiquitous presence in the environment contributes to broad and continuous human exposure, which has been associated with deleterious health effects. Despite numerous controversial discussions and a lack of consensus about BPA's safety, growing evidence indicates that BPA exposure positively correlates with an increased risk of developing obesity. An updated analysis of the epidemiological, in vivo, and in vitro studies indicates that BPA should be considered an obesogenic environmental compound. Precisely, BPA exposure during all life stages correlates with increased body weight and/or body mass index. Developmental periods that include prenatal, infancy, and childhood appear to be critical windows with increased sensitivity to BPA effects. Finally, blood analysis and in vitro data clearly demonstrate that BPA promotes adipogenesis, lipid and glucose dysregulation, and adipose tissue inflammation, thus contributing to the pathophysiology of obesity. Future prevention efforts should now be employed to avoid BPA exposure, and more research to determine in depth the critical time windows, doses, and impact of long-term exposure of BPA is warranted in order to clarify its risk assessment.

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Section: Figurementioning

confidence: 99%

“…Bisphenol A (BPA) that has been used widely as a raw material in the production of polycarbonates and epoxy resins is known as an endocrine disruptor mimicking the biological activity of estrogen. [1][2][3] Because of the colorless nature owing to the wide gap (ca. 4.3 eV) between the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO), it is impossible to discern toxic BPA dissolved in solution with eyes, as shown in Figure 1(a).…”

mentioning

confidence: 99%

Facile and Rapid Visualization of Colorless Endocrine Disruptor Bisphenol A by Interfacial Charge‐Transfer Transitions with TiO₂ Nanoparticles

2017

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Bisphenol A (BPA) is an estrogen‐mimicking endocrine disruptor, which has been widely used in the production of polycarbonates and epoxy resins. Because BPA is a colorless material owing to the wide HOMO‐LUMO gap of ca. 4.3 eV, we cannot discern toxic BPA dissolved in solution with eyes. Here, we report a facile and rapid method for visible‐light sensing of BPA with TiO2 nanoparticles. The chemical adsorption of BPA on anatase TiO2 nanoparticles via the two phenol groups induces interfacial charge‐transfer (ICT) transitions from BPA to TiO2 in the visible region. The ICT transitions give rise to visible‐light absorption up to ca. 600 nm, allowing visible‐light sensing of BPA. This method is also applicable to other phenol‐containing endocrine disruptors. More generally, to our best knowledge, this is the first demonstration for visible‐light sensing of colorless toxic organic compounds based on ICT transitions.

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Bisphenol A, obesity, and type 2 diabetes mellitus: genuine concern or unnecessary preoccupation?

Cited by 61 publications

References 54 publications

Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

Is bisphenol A an environmental obesogen?

Facile and Rapid Visualization of Colorless Endocrine Disruptor Bisphenol A by Interfacial Charge‐Transfer Transitions with TiO₂ Nanoparticles

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Bisphenol A, obesity, and type 2 diabetes mellitus: genuine concern or unnecessary preoccupation?

Cited by 61 publications

References 54 publications

Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

Is bisphenol A an environmental obesogen?

Facile and Rapid Visualization of Colorless Endocrine Disruptor Bisphenol A by Interfacial Charge‐Transfer Transitions with TiO2 Nanoparticles

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Product

Resources

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Facile and Rapid Visualization of Colorless Endocrine Disruptor Bisphenol A by Interfacial Charge‐Transfer Transitions with TiO₂ Nanoparticles