Content area
Full text
Introduction
Over the past decade, the incidence of diabetes has increased dramatically. The WHO estimates mortality due to diabetes to increase by 50% in the next 10 y, making it a major cause of death by 2030 and placing a substantial economic burden on the health care system globally (Mathers and Loncar 2006; American Diabetes Association 2013). Therefore, understanding the underlying factors of this global epidemic is critical. It has been well established that factors such as food intake and sedentary lifestyle significantly influence the incidence of diabetes. Although these are important factors, changes in our lifestyle have also increased our exposure to a variety of synthetic chemicals that are linked to various diseases such as diabetes and obesity in experimental models and human epidemiological studies (Alonso-Magdalena et al. 2015b; Jašarević et al. 2011; Lang et al. 2008; Newbold et al. 2008).
Bisphenol A (BPA) is one such synthetic chemical to which we are ubiquitously exposed through food, drink, and skin contact (Stahlhut et al. 2009). Detectable amounts of BPA are found in urine samples of populations from around the world (Nahar et al. 2012; Stahlhut et al. 2009; Zhang et al. 2011). Exposure to BPA has been associated with prediabetes and type 2 diabetes in human cross sectional (Aekplakorn et al. 2015; Ahmadkhaniha et al. 2014; Sabanayagam et al. 2013; Shankar and Teppala 2011) and longitudinal studies (Sun et al. 2014). Such associations have been further confirmed using animal models of exposure during adulthood (Alonso-Magdalena et al. 2006; Batista et al. 2012).
The pancreas undergoes substantial remodeling during late gestation and early neonatal life. This involves formation of new β cells by differentiation of precursor cells during late gestation (Hellerstrom et al. 1988) followed by substantial remodeling, including high rates of replication and cell death in the neonatal period (Finegood et al. 1995; Scaglia et al. 1995, 1997; Swenne 1983). The β-cell replication rate gradually declines (Finegood et al. 1995; Swenne 1983), and post-weaning β-cell turnover is regulated by β-cell death and very slow rates of replication (Bouwens and Rooman 2005; Scaglia et al. 1995). An exposure to synthetic chemicals such as BPA during this vulnerable period is even more concerning because of the potential to not only alter normal fetal development, but also to...