Department of Biology and Chemistry, City University of Hong Kong, Hong Kong, China.
Croucher Institute for Environmental Sciences, Partner State Key Laboratory of Environmental and Biological Analysis, Department of Biology, Hong Kong Baptist University, Hong Kong, China.
Environ Pollut. 2016 Nov;218:923-930. doi: 10.1016/j.envpol.2016.08.039. Epub 2016 Aug 21.
Mounting evidence has shown that an alteration of the gut microbiota is associated with diet, and plays an important role in animal health and metabolic diseases. However, little is known about the influence of environmental contaminants on the gut microbial community. Bisphenol A (BPA), which is widely used for manufacturing plastic products, has recently been classified as an environmental obesogen. Although many studies have demonstrated the metabolic-disrupting effects of BPA on liver and pancreatic functions, the possible effects of this synthetic compound on the metabolic diversity of the intestinal microbiota is unknown. Using 16S rRNA gene sequencing analysis on caecum samples of CD-1 mice, the present study aimed to test the hypothesis that dietary BPA intake may influence the gut microbiota composition and functions, an important attributing factor to development of the metabolic syndrome. A high-fat diet (HFD) and high-sucrose diet (HSD) were included as the positive controls for comparing the changes in the intestinal microbial profiles. Our results demonstrated a significant reduction of species diversity in the gut microbiota of BPA-fed mice. Alpha and beta diversity analyses showed that dietary BPA intake led to a similar gut microbial community structure as that induced by HFD and HSD in mice. In addition, comparative analysis of the microbial communities revealed that both BPA and a HFD favored the growth of Proteobacteria, a microbial marker of dysbiosis. Consistently, growth induction of the family Helicobacteraceae and reduction of the Firmicutes and Clostridia populations were observed in the mice fed BPA or a HFD. Collectively, our study highlighted that the effects of dietary BPA intake on the shift of microbial community structure were similar to those of a HFD and HSD, and revealed microbial markers for the development of diseases associated with an unstable microbiota.
越来越多的证据表明,肠道微生物群的改变与饮食有关,并在动物健康和代谢疾病中发挥着重要作用。然而,人们对环境污染物对肠道微生物群落的影响知之甚少。双酚 A(BPA)广泛用于制造塑料制品,最近被归类为环境内分泌干扰物。尽管许多研究表明 BPA 对肝脏和胰腺功能有代谢干扰作用,但这种合成化合物对肠道微生物代谢多样性的可能影响尚不清楚。本研究使用 CD-1 小鼠盲肠样本的 16S rRNA 基因测序分析,旨在检验以下假设:饮食中 BPA 的摄入可能会影响肠道微生物群落的组成和功能,这是代谢综合征发展的一个重要归因因素。高脂肪饮食(HFD)和高蔗糖饮食(HSD)被纳入阳性对照组,以比较肠道微生物谱的变化。我们的研究结果表明,BPA 喂养组小鼠肠道微生物群的物种多样性显著降低。α和β多样性分析表明,饮食中 BPA 的摄入导致肠道微生物群落结构与 HFD 和 HSD 诱导的结构相似。此外,微生物群落的比较分析表明,BPA 和 HFD 均有利于变形菌的生长,变形菌是肠道微生态失调的微生物标志物。一致地,在 BPA 或 HFD 喂养的小鼠中观察到 Helicobacteraceae 家族的生长诱导和厚壁菌门和梭菌属种群的减少。总之,我们的研究强调了饮食中 BPA 摄入对微生物群落结构变化的影响与 HFD 和 HSD 相似,并揭示了与不稳定微生物群相关疾病发展的微生物标志物。