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ABSTRACT:
PROVIDER: PRJNA828117 | ENA |
REPOSITORIES: ENA
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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.
2022-02-22 | PXD009564 | Pride
Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids and regulates bile acid metabolism, glucose and cholesterol homeostasis. From mouse studies we know that the novel FXR agonist obeticholic acid (OCA) regulates expression of many genes in the liver, but there is currently no data on the effects of OCA on human liver gene expression. This is especially relevant since the novel FXR agonist OCA is currently tested in clinical trials for the treatment of several diseases, such as nonalcoholic steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD) and Type 2 Diabetes. In this study we investigate the effect of OCA treatment on gene expression profiles and localization of FXR to the genome in relevant liver samples. ChIP-Seq for FXR in Liver tissue from 2 male mice treated with OCA/INT-747 (10mg/kg/day) and 2 male mice treated with vehicle (1% methyl cellulose).
2016-01-27 | E-GEOD-73624 | biostudies-arrayexpress
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Gut microbiota alternations by PED infection
| PRJEB8875 | ENA
Project description:Background: The increasing prevalence of chronic liver disease has become a significant global health concern. Pyroptosis leads to cell rupture, releasing large amounts of pro-inflammatory cellular contents and promoting the progression of liver fibrosis. Therefore, targeting pyroptosis may serve as a new strategy for the treatment of chronic liver diseases. Methods: We constructed GSDMD-NTki/wt & Alb-creki/wt mice using CRISPR/Cas9 gene editing technology and induced conditional cell death by doxycycline to construct a mouse model of liver fibrosis. We analyzed differentially expressed genes by RNA sequencing and explored their biological functions. Obeticholic acid was used to assess the modeling effects of fibrosis. Results: Doxycycline-treated GSDMD-NTki/wt & Alb-creki/wt mice showed severe liver damage, vacuolation of hepatocytes, increased collagen fibers, accumulation of lipid droplets, and much stronger expression of genes involved in liver fibrosis development in the liver compared with untreated mice. RNA-sequencing showed that upregulated differentially expressed genes in the GSDMD-NTki/wt & Alb-creki/wt doxycycline-treated group were involved in inflammatory responses, cell activation, and metabolic processes. Obeticholic acid was used to assess the modeling effects of fibrosis. Obeticholic acid treatment of GSDMD-NTki/wt & Alb-creki/wt mice reduced ALT and AST levels, and enhanced anti-fibrotic effects were observed. Conclusions: Our results demonstrated that we successfully constructed a mouse model of liver fibrosis, and GSDMD-NT induced fibrosis by mediating lipid metabolism.
2025-01-11 | GSE252989 | GEO
Project description:Emerging evidence indicates that selective nutrient restriction can reproduce metabolic benefits. Although methionine and branched-chain amino acid limitation improve metabolism and reshape the gut microbiome, the effects of other nutrients are still unclear. In this study, we examine the consequences of restricting methionine, tryptophan, and niacin, and find that their transient deprivation induces significant changes in gut microbiota.
2025-07-12 | GSE300499 | GEO