Department of Environmental and Global Health, University of Florida, Gainesville, FL, USA; Center for Environmental and Human Toxicology, University of Florida, Gainesville, FL, USA.
Center for Environmental and Human Toxicology, University of Florida, Gainesville, FL, USA; Department of Anthropology, University of Florida, Gainesville, FL, USA.
Environ Pollut. 2020 Oct;265(Pt B):114496. doi: 10.1016/j.envpol.2020.114496. Epub 2020 Apr 3.
Microbiome community structure is intimately involved in key biological functions in the gastrointestinal (GI) system including nutrient absorption and lipid metabolism. Recent evidence suggests that disruption of the GI microbiome is a contributing factor to metabolic disorders and obesity. Poor diet and chemical exposure have been independently shown to cause disruption of the GI microbiome community structure and function. We hypothesized that the addition a chemical exposure to overfeeding exacerbates adverse effects on the GI microbiome community structure and function. To test this hypothesis, adult zebrafish were fed a normal feeding regime (Control), an overfeeding regime (OF), or an overfeeding regime contaminated with diethylhexyl phthalate (OF + DEHP), a suspected obesogen-inducing chemical. After 60 days, fecal matter was collected for sequencing, identification, and quantification of the GI microbiome using the 16s rRNA hypervariable region. Analysis of beta diversity indicated distinct microbial profiles between treatments with the largest divergence between Control and OF + DEHP groups. Based upon functional predictions, OF + DEHP treatment altered carbohydrate metabolism, while both OF and OF + DEHP affected biosynthesis of fatty acids and lipid metabolism. Co-occurrence network analysis revealed decreases in cluster size and a fracturing of the microbial community network into unconnected components and a loss of keystone species in the OF + DEHP treatment when compared to Control and OF treatments. Data suggest that the addition of DEHP in the diet may exacerbate microbial dysbiosis, a consequence that may explain in part its role as an obesogenic chemical.
微生物群落结构与胃肠道 (GI) 系统中的关键生物学功能密切相关，包括营养吸收和脂质代谢。最近的证据表明，GI 微生物群落的破坏是代谢紊乱和肥胖的一个促成因素。不良饮食和化学暴露已被独立证明会导致 GI 微生物群落结构和功能的破坏。我们假设，在过度喂养的基础上增加化学暴露会加剧对 GI 微生物群落结构和功能的不利影响。为了验证这一假设，成年斑马鱼被喂食正常喂养方案 (Control)、过度喂养方案 (OF) 或过度喂养方案加邻苯二甲酸二己酯 (OF + DEHP)，邻苯二甲酸二己酯是一种可疑的肥胖诱导化学物质。60 天后，收集粪便用于测序，使用 16s rRNA 高变区鉴定和定量 GI 微生物群落。β多样性分析表明，处理之间存在明显的微生物特征，Control 和 OF + DEHP 组之间的差异最大。基于功能预测，OF + DEHP 处理改变了碳水化合物代谢，而 OF 和 OF + DEHP 均影响脂肪酸的生物合成和脂质代谢。共现网络分析表明，与 Control 和 OF 处理相比，OF + DEHP 处理中群落大小减小，微生物群落网络破碎成不相连的成分，并且关键物种丢失。数据表明，饮食中添加 DEHP 可能会加剧微生物失调，这可能部分解释了它作为肥胖诱导化学物质的作用。
