الفهرس 
Bisphenol A (BPA).Only 14 pages are availabe for public view
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Abstract
Bisphenol A (BPA), is one of the highest volume chemicals produced worldwide. It is used to manufacture polymeric materials used for a variety of consumer products. These polymers include epoxy resins that are used to line food cans and polycarbonate plastics used in dental composites and sealants, water storage tanks, and baby bottles. The exposure occurs primarily through the consumption of food and beverage cans that have been contaminated with BPA.BPA is considered as one of the environmental obesogens which are characterized by a foreign chemical compounds that disrupt normal development and balance of lipid metabolism. It may also disrupt energy balance or modify the regulation of appetite and satiety to enhance fat accumulation and obesity. BPA can mimic endogenous hormones, subsequently disturb endocrine function. BPA has a strong binding affinity for the transmembrane estrogen receptor (ER), G-protein-coupled receptor 30 (GPR30), and estrogen-related receptor (ERR). It can activate transcription factors, such as peroxisome proliferator-activated receptors PPARs and the aryl hydrocarbon receptor (AhR). Therefore, it is considered as an environmental obesogenic through promoting adipogenesis, lipid accumulation and acts as endocrinal disrupting chemicals (EDCs) altering adipokine hormone release.
The present study was carried out to evaluate the effects of BPA on lipid profile and lipid metabolism and clarifying the role of adiponectin hormone and peroxisome proliferator-activated receptor gamma (PPARγ) genotyping that have impacts on lipid metabolism in modulation of metabolism and BPA exposure.
Therefore, this study was conducted to estimate the effects of BPA on lipid profile between two groups (obese and non-obese women) and across three percentiles of BPA concentrations, to elucidate the mechanism of action by which it acts as an obesogen and disrupts lipid metabolism through determination of serum adipokines hormones (adiponectin and leptin), glucose homeostasis, and to reveal the role of PPARγ genotyping.
The results showed a disturbed lipid profile, as the BPA generated a clear U shaped response across the three studied percentiles with significant differences across these percentiles with increased levels at the highest and lowest percentiles (cholesterol and LDL-c) and TG showed the same pattern but with insignificant differences while the HDL-c mean level showed an inverted U-shaped pattern and there were no significant differences across the percentiles
Also, this study revealed significant differences across the percentiles generating clear U shape pattern for the BMI and WC, which indicated that BPA was associated with general and central obesity.
Adipokine hormones (adiponectin and leptin) did not show any statistically significant difference across the three percentiles with suppressive effects across the percentiles for adiponectin.
The impact of BPA on glucose hemostasis was declared as decreased in FBS and increased in level of insulin. Moreover, HOMA-IR formula showed the highest insulin resistance at the moderate percentile of BPA group but the mean levels of these parameters did not show any significance across these percentiles.
The result of the present study showed that there was no mutation detected at position 12 which indicated that Pro12Ala genotype was not associated with BMI and with the different concentration of BPA as well as the obesity-related metabolic syndrome among the study population of the study population.
In conclusion, BPA generated a clear response in which the general obesity (BMI) and the central obesity (WC) showed significant increase at the low and high percentiles. Moreover, BPA had a disturbed action on lipid profile and suppressive effect on adiponectin release which support the claim the BPA as endocrine disruptor may increase the risk of developing obesity associated disorder such as glucose intolerance, hyperinsulimia, hypertension and increasing the risk of diabetes and cardiovascular disease.