双酚A对脂代谢和肥胖的影响及其机制的研究进展

Research advances in association of bisphenol A exposure with lipid metabolism and obesity

近年来,肥胖及糖尿病、高脂血症和高血压等代谢综合征患者不断增加,已成为严重的社会公共健康问题。研究表明,肥胖可能是基因、行为以及环境因素相互作用的结果。围生期或青春期暴露于双酚A均可导致体质量增加。人群流行病学研究也发现,双酚A暴露与肥胖和2型糖尿病相关。围生期暴露于双酚A可以使脂肪细胞分化提前,这可能与基因表达变异有关。双酚A引起肥胖的可能机制包括直接与雌激素受体结合,起激动剂或拮抗剂的作用。双酚A也能通过阻碍酶活性或激活P450酶等途径产生间接作用。本文重点探讨以环境雌激素双酚A为代表的环境内分泌干扰物与肥胖发生发展的关系。通过综述双酚A与肥胖的关系,为预防和控制肥胖提供实验和理论依据。

The incidence of adult obesity, diabetes, hyperlipidemia and hypertention has been rising dramatically in recent years. Obesity and overweight have become a significant public health problem worldwide. Though obesity is caused by complex interactions between genetic, behavioral, and environ- mental factors, its etiology is still unclear. There is growing evidence that exposure to bisphenol A （BPA） during prenatal and neonatal or adolescence periods leads to much body mass gain. In addition, in epidemiological studies, the association between BPA exposure and obesity and type 2 diabetes has been found. The potential mechanism may be attributed to promoted differentiation and function in adipocytes via alteration of a number of genes. BPA may act also through other mechanisms. It can directly bind to nuclear receptors acting as agonists or antagonists and indirectly disrupt hormone levels by inhibiting enzymatic activity or by activating expression of the P450 enzymes. This review is focused on the effects of estrogenic endocrine disrupting chemicals such as BPA on the development of obesity.