Bisphenol A and Type 2 Diabetes Mellitus: A Review of Epidemiologic, Functional, and Early Life Factors.

Josanne Vassallo,Francesca Farrugia,Nikolai Paul Pace,Alexia Aquilina

doi:10.3390/ijerph18020716

Josanne Vassallo, Francesca Farrugia

Open Access

https://doi.org/10.3390/ijerph18020716

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Abstract

Type 2 diabetes mellitus (T2DM) is characterised by insulin resistance and eventual pancreatic β-cell dysfunction, resulting in persistent high blood glucose levels. Endocrine disrupting chemicals (EDCs) such as bisphenol A (BPA) are currently under scrutiny as they are implicated in the development of metabolic diseases, including T2DM. BPA is a pervasive EDC, being the main constituent of polycarbonate plastics. It can enter the human body by ingestion, through the skin, and cross from mother to offspring via the placenta or breast milk. BPA is a xenoestrogen that alters various aspects of beta cell metabolism via the modulation of oestrogen receptor signalling. In vivo and in vitro models reveal that varying concentrations of BPA disrupt glucose homeostasis and pancreatic β-cell function by altering gene expression and mitochondrial morphology. BPA also plays a role in the development of insulin resistance and has been linked to long-term adverse metabolic effects following foetal and perinatal exposure. Several epidemiological studies reveal a significant association between BPA and the development of insulin resistance and impaired glucose homeostasis, although conflicting findings driven by multiple confounding factors have been reported. In this review, the main findings of epidemiological and functional studies are summarised and compared, and their respective strengths and limitations are discussed. Further research is essential for understanding the exact mechanism of BPA action in various tissues and the extent of its effects on humans at environmentally relevant doses.

Highlights

Type 2 diabetes mellitus (T2DM) is a common chronic metabolic disorder characterised by peripheral insulin resistance, β-cell dysfunction and an inadequate compensatory insulin secretory response [1]
The findings from this study suggest that foetal exposure to low-dose bisphenol A (BPA) is more likely to affect a sensitive subpopulation characterised by early life growth restriction and rapid catchup growth post weaning, which could be at higher risk for the development of T2DM [94]
The extensive body of evidence outlined above provides insight into the multiple mechanisms through which BPA, as a xenoestrogen, modulates physiological pathways linked to the development of T2DM

Summary

Introduction

Type 2 diabetes mellitus (T2DM) is a common chronic metabolic disorder characterised by peripheral insulin resistance, β-cell dysfunction and an inadequate compensatory insulin secretory response [1]. The disorder has an underlying complex aetiology, with several established risk factors including sedentary lifestyle, calorie dense diets, visceral adiposity and a broad array of both common and rare genetic variants [4,5,6]. In addition to these classical risk factors, an increasing body of evidence implicates environmental chemicals in the rising epidemic of T2DM. Bisphenol A (BPA) is a widespread EDC that is the main constituent of polycarbonate plastics. The primary route of human exposure to BPA is oral, and over 90% of individuals have detectable urine BPA levels even though it is

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