Ontology highlight
ABSTRACT:
PROVIDER: PRJNA690735 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243 Total RNA obtained from adipose tissue of wt- or IL15-KO mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
2014-07-01 | E-GEOD-55057 | biostudies-arrayexpress
Project description:By fermenting dietary fiber, the gut microbiota supplies carbon to host epithelial cells in the form of short-chain fatty acids and other metabolic byproducts. To track the transfer of carbon from fiber to host tissues via the microbiota and more clearly define the molecules mediating this transfer, we conducted stable isotope tracing in mice with U-13C-labeled inulin followed by untargeted metabolomics by LC-MS. Additionally, we applied this labeling approach to mice with chemically induced colitis to examine how inflammation impacts carbon transfer from the microbiota to host tissues, which may aid in understanding the development of inflammatory bowel diseases.
2021-07-04 | MSV000087752 | MassIVE
Project description:Altered Tongue Coating Microbiota in Inflammatory Bowel Diseases patients contributes to intestinal inflammation
| PRJNA1103394 | ENA
Project description:Salivary microbiome associated with inflammatory bowel diseases
| PRJNA414682 | ENA
Project description:Imbalance in beneficial and harmful bacteria underlies gastrointestinal diseases, such as inflammatory bowel disease. Here, we demonstrated that certain E. coli strains, specifically adherent-invasive E. coli (AIEC), utilize a serine metabolism pathway to outcompete other E. coli strains in the inflamed gut. In contrast, amino acid metabolism has a minimal effect on their competitive fitness in the healthy gut. The availability of luminal serine used for the competition of E. coli is largely dependent on dietary intake, as the inflammation-induced blooms of AIEC are significantly blunted when amino acids, particularly serine, are removed from the diet. Thus, intestinal inflammation regulates the intraspecific competition between Enterobacteriaceae by eliciting their metabolic reprogramming.
2019-09-06 | GSE106412 | GEO
Project description:Inflammatory Bowel Diseases are associated with marked alterations of IECs with a subsequent loss of barrier function. To identify alterations in signaling pathways in intestinal epithelium upon inflammation, we analyzed the transcriptome of IECs from patients suffering from Crohn’s disease.
2015-12-01 | GSE72780 | GEO
Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
2014-07-01 | GSE55057 | GEO
Project description:The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine1. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro2, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century3. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.
In Study Design factor “Treatment” CMC stands for carboxymethylcellulose and P80 for polysorbate-80
Research is published:
http://www.nature.com/nature/journal/v519/n7541/full/nature14232.html
2015-06-11 | ST000203 | MetabolomicsWorkbench
Project description:The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine1. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro2, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century3. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.
In metadata factor “Treatment” CMC stands for carboxymethylcellulose and P80 for polysorbate-80
Research is published:
http://www.nature.com/nature/journal/v519/n7541/full/nature14232.html
2015-06-12 | ST000213 | MetabolomicsWorkbench