Alonso-Magdalena Paloma, Rivera Francisco J, Guerrero-Bosagna Carlos
Departamento de Biología Aplicada, Universidad Miguel Hernández, Elche, Spain.
Laboratory of Stem Cells and Neuroregeneration, Institute of Anatomy, Histology and Pathology, Faculty of Medicine and Center for Interdisciplinary Studies on the Nervous System (CISNe), Universidad Austral de Chile, Valdivia, Chile.
Environ Epigenet. 2016 Oct 21;2(3):dvw022. doi: 10.1093/eep/dvw022. eCollection 2016 Aug.
Exposure to environmental toxicants is now accepted as a factor contributing to the increasing incidence of obesity and metabolic diseases around the world. Such environmental compounds are known as 'obesogens'. Among them, bisphenol-A (BPA) is the most widespread and ubiquitous compound affecting humans and animals. Laboratory animal work has provided conclusive evidence that early-life exposure to BPA is particularly effective in predisposing individuals to weight gain. Embryonic exposure to BPA is reported to generate metabolic disturbances later in life, such as obesity and diabetes. When BPA administration is combined with a high-fat diet, there is an exacerbation in the development of metabolic disorders. Remarkably, upon BPA exposure of gestating females, metabolic disturbances have been found both in the offspring and later in life in the mothers themselves. When considering the metabolic effects generated by an early developmental exposure to BPA, one of the questions that arises is the role of precursor cells in the etiology of metabolic disorders. Current evidence shows that BPA and other endocrine disruptors have the ability to alter fat tissue development and growth by affecting the capacity to generate functional adipocytes, as well as their rate of differentiation to specific cell types. Epigenetic mechanisms seem to be involved in the BPA-induced effects related to obesity, as they have been described in both and models. Moreover, recent reports also show that developmental exposure to BPA generates abnormalities that can be transmitted to future generations, in a process called as transgenerational epigenetic inheritance.
如今，接触环境毒物已被公认为是导致全球肥胖和代谢疾病发病率上升的一个因素。这类环境化合物被称为“致肥胖物”。其中，双酚A（BPA）是影响人类和动物的最广泛、最普遍的化合物。实验动物研究已提供确凿证据，表明生命早期接触BPA在使个体易患体重增加方面特别有效。据报道，胚胎期接触BPA会在生命后期引发代谢紊乱，如肥胖和糖尿病。当给动物施用BPA并搭配高脂饮食时，代谢紊乱的发展会加剧。值得注意的是，在妊娠雌性动物接触BPA后，在其后代以及母体自身的生命后期都发现了代谢紊乱。在考虑早期发育接触BPA所产生的代谢影响时，出现的问题之一是前体细胞在代谢紊乱病因学中的作用。目前的证据表明，BPA和其他内分泌干扰物能够通过影响产生功能性脂肪细胞的能力及其向特定细胞类型的分化速率来改变脂肪组织的发育和生长。表观遗传机制似乎参与了与肥胖相关的BPA诱导效应，这在动物和人类模型中均有描述。此外，最近的报告还表明，发育过程中接触BPA会产生可传递给后代的异常，这一过程称为跨代表观遗传遗传。
