PDF(Pubmed)
Abstract：
A very low calorie ketogenic diet (VLCKD) impacts host metabolism in people marked by an excess of visceral adiposity, and it affects the microbiota composition in terms of taxa presence and relative abundances. As a matter of fact, there is little available literature dealing with microbiota differences in obese patients marked by altered intestinal permeability. With the aim of inspecting consortium members and their related metabolic pathways, we inspected the microbial community profile, together with the set of volatile organic compounds (VOCs) from untargeted fecal and urine metabolomics, in a cohort made of obese patients, stratified based on both normal and altered intestinal permeability, before and after VLCKD administration. Based on the taxa relative abundances, we predicted microbiota-derived metabolic pathways whose variations were explained in light of our cohort symptom picture. A totally different number of statistically significant pathways marked samples with altered permeability, reflecting an important shift in microbiota taxa. A combined analysis of taxa, metabolic pathways, and metabolomic compounds delineates a set of markers that is useful in describing obesity dysfunctions and comorbidities.
摘要：
低热量的生酮饮食（VLCKD）会影响以内脏肥胖过多为特征的人的宿主代谢，并且它在分类群的存在和相对丰度方面影响微生物群的组成。事实上,关于肠道通透性改变的肥胖患者微生物群差异的文献很少.为了检查联盟成员及其相关的代谢途径，我们检查了微生物群落概况，与来自非靶向粪便和尿液代谢组学的挥发性有机化合物（VOCs）一起，在由肥胖患者组成的队列中，根据正常和改变的肠道通透性进行分层，VLCKD给药前后。根据分类群的相对丰度，我们预测了源自微生物群的代谢途径,根据我们的队列症状图片对其变化进行了解释.完全不同数量的具有统计学意义的途径标记了渗透率改变的样品，反映了微生物群的重要转变。对分类群的综合分析，代谢途径，和代谢组学化合物描绘了一组标记，可用于描述肥胖功能障碍和合并症。
