Bisphenol-A (BPA), a widespread endocrine-disrupting chemical, has been recognized as a risk factor for metabolic disorders. BPA is considered to be involved in the impairment of carbohydrate and lipid metabolism but the underlying mechanisms still need to be elucidated. Present study was aimed to investigate the impact of BPA exposure on enzymatic and metabolic pathways that are responsible to regulate the carbohydrate and lipid metabolism. Experimental rats were exposed to different doses of BPA (50, 500, 2500 and 5000 μg/kg/day orally) dissolved in 1.5% dimethyl sulfoxide for a period of 3 months. Serum level of key metabolic enzymes (α-amylase, α-glucosidase, hexokinase, glucose-6-phosphatase and HMG-CoA-reductase) was measured by ELISA method. BPA-exposure suppressed the mRNA expression of gene encoding insulin resulting in poor insulin production. While hexokinase, acetyl-CoA carboxylase and squalene epoxide were up-regulated upon BPA exposure that justified the increased lipid profile. Moreover, BPA exposure showed considerably decreased glucose uptake through insulin signaling via Akt/GLUT4 pathways. There was a significant (p < 0.001) reduction in tissue level of glucose transporters. BPA significantly (p < 0.001) decreased the serum levels of oxidative stress biomarkers (GSH, CAT, and SOD). Serum levels of leptin, TNF-α, and IL-6 were rapidly increased upon exposure to BPA (p < 0.001). It was clearly evident from this study that BPA disturbed the carbohydrate and lipid metabolism after chronic exposure. It also accelerated the inflammatory processes by increasing the oxidative stress which ultimately lead towards the insulin resistance and impaired carbohydrate and lipid metabolism.

双酚A（BPA）是一种广泛的破坏内分泌的化学物质，已被认为是代谢紊乱的危险因素。BPA被认为与碳水化合物和脂质代谢的损害有关，但其潜在机制仍需阐明。本研究旨在调查BPA暴露对负责调节碳水化合物和脂质代谢的酶和代谢途径的影响。实验大鼠暴露于溶于1.5％二甲基亚砜的不同剂量的BPA（50、500、2500和5000μg/ kg /天口服）持续3个月。通过ELISA法测定血清中关键代谢酶（α-淀粉酶，α-葡萄糖苷酶，己糖激酶，葡萄糖-6磷酸酶和HMG-CoA还原酶）的水平。BPA暴露抑制了编码胰岛素的基因的mRNA表达，导致胰岛素产生不良。虽然己糖激酶，乙酰辅酶A羧化酶和角鲨烯环氧化合物在BPA暴露后被上调，这证明脂质分布增加。此外，BPA暴露显示通过Akt / GLUT4途径通过胰岛素信号传导的葡萄糖摄取大大降低。葡萄糖转运蛋白的组织水平显着降低（p <0.001）。BPA显着（p <0.001）降低了血清氧化应激生物标志物（GSH，CAT和SOD）的水平。血清中瘦素，TNF-α和IL-6的水平在接触BPA后迅速增加（p <0.001）。从这项研究中可以明显看出，BPA长期暴露后会干扰碳水化合物和脂质的代谢。