The effect of environmental estrogens exposure on oxidative stress and dyslipidemia, and their impact on insulin sensitivity

Bisphenol A and S (BPA and BPS), chemicals used in food packaging, have been closely associated with insulin resistance. However, the mechanism by which BPA and BPS induces type 2 diabetes is debatable. The aim of this study was to investigate if oxidative stress mediates BPA and BPS’s effect on lipid profiles and glucose uptake via insulin and aerobic exercise. Normal weight and overweight/obese subjects participated in 2 separate testing days. On both days, blood glucose was measured before 50 g of maltodextrin consumption and following 30-, 60-, and 75-minutes. On the “Exercising” testing day, subjects ran for 30-minutes at 70% of maximal heart rate; while on the “Resting” day, they remained seated. Urinary BPA, BPS, 8-isoprostane (an oxidative stress marker), creatinine, lipid profile, body fat percentage and physical fitness were measured. The exercise condition produced a decrease in blood glucose during the 30-60-minute protocol interval within normal and overweight/obese subjects when compared to the resting day. Blood glucose of both experimental days was negatively associated with body fat (r=-0.58) only. Urinary BPA and BPS were positively associated with oxidative stress (r = 0.62 and 0.82, respectively). BPA and oxidative stress were negatively associated with physical fitness (r=-45 and − 0,5, respectively), while BPS and oxidative stress were associated with increased triglycerides (r = 0.47 and 0.49, respectively). Oxidative stress mediates the effect of BPA and BPS on risk factors related to T2D development. Thus, modulating oxidative stress could be a valuable strategy to attenuate the effect of bisphenols in the human body.