Project description:Analysis of breast cancer survivors' gut microbiota after lifestyle intervention, during the COVID-19 lockdown, by 16S sequencing of fecal samples.
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
Project description:The mouse stool samples were collected from different diets fed mice and bacterial cells were harvest for metaproteomic analysis for understanding the role ofdiet on gut microbiota.
Project description:Gut microbiota comparation of Young mice (n=10), Old mice, Young_yFMT (Young mice 14 days after transplant feces from young mice, n=10) and Young_oFMT (Young mice 14 days after transplant feces from old mice, n=10), Antibiotic group (Cefazolin, n=8).
Project description:Gut microbiota has profound effects on obesity and associated metabolic disorders. Targeting and shaping the gut microbiota via dietary intervention using probiotics, prebiotics and synbiotics can be effective in obesity management. Despite the well-known association between gut microbiota and obesity, the microbial alternations by synbiotics intervention, especially at the functional level, are still not characterized. In this study, we investigated the effects of synbiotics on high fat diet (HFD)-induced metabolic disorders, and systematically profiled the microbial profile at both the phylogenetic and functional levels. Synbiotics significantly reversed the HFD-induced change of microbial populations at the levels of richness, taxa and OTUs. Potentially important species Faecalibaculum rodentium and Alistipes putredinis that might mediate the beneficial effects of synbiotics were identified. At the functional level, short chain fatty acid and bile acid profiles revealed that interventions significantly restored cecal levels of acetate, propionate, and butyrate, and synbiotics reduced the elevated total bile acid level. Metaproteomics revealed the effect of synbiotics might be mediated through pathways involved in carbohydrate, amino acid, and energy metabolisms, replication and repair, etc. These results suggested that dietary intervention using our novel synbiotics alleviated HFD-induced weight gain and restored microbial ecosystem homeostasis phylogenetically and functionally.
Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).