Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1135911 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29826804_1.fastq.gz | Fastqsanger.gz | |||
| SRR29826804_2.fastq.gz | Fastqsanger.gz | |||
| SRR29826805_1.fastq.gz | Fastqsanger.gz | |||
| SRR29826805_2.fastq.gz | Fastqsanger.gz | |||
| SRR29826806_1.fastq.gz | Fastqsanger.gz |
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Project description:Specific gut microbiota is critically involved in metabolic diseases, including obesity. Through analysis of gut microbiota in diabetic patients and animal models, it was found that Romboutsia ilealis is closely associated with obesity. Here, our findings show that oral administration of Romboutsia ilealis significantly alleviates diet-induced obesity and metabolic dysfunction. Interestingly, this effect occurs not through modulation of food intake or energy expenditure, but by regulating lipid absorption and metabolism in the gut. Additionally, metabolomics analysis identified 2-oxindole-3-acetic acid (OAA) as the key metabolite involved in the regulation of obesity by Romboutsia ilealis. Its regulatory effect on intestinal lipid absorption was further validated both in vitro and in vivo. Mechanistically, using biotin-labeled OAA combined with proteomic analysis, we found that OAA directly interacts with the deubiquitin enzyme PSMD3, increasing the ubiquitination level of m6A binding protein YTHDF2 and reducing its protein stability, thereby enhancing intestinal lipid absorption. Furtherly, through m6A-seq, we discovered that YTHDF2 negatively regulates the expression of RXRB by recognizing the m6A sites on its mRNA, which in turn downregulates the expression of lipid absorption and transport proteins CD36 and FABP2, ultimately inhibiting intestinal lipid absorption. In summary, our findings reveal that Romboutsia ilealis and OAA regulate obesity-associated lipid accumulation through PSMD3-mediated deubiquitination of YTHDF2, suggesting that they represent novel prebiotics and probiotics with potential as therapeutic agents against obesity.
2024-12-19 | GSE284540 | GEO
Project description:Background and Aims: Many inflammatory diseases are associated with microbial dysbiosis, which may considerably alter the production of short-chain fatty acids (SCFAs). SCFAs are produced in the large bowel through bacterial fermentation of dietary fiber and play an important role in maintaining gut homeostasis. SCFAs, particularly acetate and butyrate, show beneficial immunomodulatory effects contributing to the prevention of inflammatory and allergic reactions. Thus, reduced production of SCFAs may impact on the mucosal immune responses critical to fighting pathogens. This study aims to determine the influence of SCFAs on a murine model of colonic bacterial infection. Methods: In the present study, we used acetate- (HAMSA) or butyrate- (HAMSB) yielding diets to deliver high concentrations of individual SCFAs to the large bowel of mice infected with C. rodentium. We assessed the effects of these SCFAs on clinical burden and gut pathogenicity in correlation with changes in bacteria growth, fecal microbiota composition, function and changes in the immunological profile. Results: Here we show in vitro that acetate and butyrate directly inhibited growth of the attaching and effacing (A/E) pathogen C. rodentium in a bacteriostatic manner. This correlated with reduced expression of Tir, a gene responsible for bacterial adherence and pathogenicity. Interestingly, HAMSA-fed mice presented reduced clinical scores during C. rodentium infection associated with high concentrations of fecal acetate. This was linked with compositional and functional changes in the microbiota when examining 16s sequencing and proteomics analysis. The HAMSA mediated is protection involved increased expression IL-22 and Muc-2 in the colon and increased numbers of CD8αα+ TCRγδ T cells in the colonic epithelium. These effects were dependent on GPR43, a metabolite-sensing GPCR that binds acetate. Conclusions: We established a promising new approach to moderate bacterial gut infections by manipulating the gut microbiota and mucosal immune tolerance through diets that yield the SCFA acetate.
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Project description:Roux-en-Y gastric bypass (RYGB) is highly effective in reversing obesity and associated diabetes. Recent observations in humans suggest a contributing role of increased circulating bile acids in mediating such effects. Here we use a diet-induced obesity mouse model and compared metabolic remission when bile flow was diverted through a gallbladder anastomosis to jejunum, ileum or duodenum (sham control). We found that only bile diversion to the ileum results in physiologic changes similar to RYGB including sustained improvements in weight, glucose tolerance and hepatic steatosis despite differential effects on hepatic gene expression. Circulating free fatty acids and triglycerides decrease while bile acids increase, particularly conjugated tauro-b-muricholic acid, an FXR antagonist. Activity of the hepatic FXR/FGF15 axis was reduced and associated with altered gut microbiota. Thus bile diversion, independent of surgical rearrangement of the gastrointestinal tract, imparts significant weight loss accompanied by improved glucose and lipid homeostasis that are hallmarks of RYGB. Total RNA from n = 5 DIO, n = 4 GB-IL, n = 5 RYGB mice livers was extracted of total RNA and submitted fro RNAseq
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2013-11-07 | E-GEOD-47760 | biostudies-arrayexpress
Project description:Gallic acid is a natural phenolic compound that displays anti-cancer properties in clinically relevant cell culture and rodent models. To date, the molecular mechanism governing the gallic acid-induced cancer cell death process is largely unclear, thus hindering development of novel therapeutics. Therefore, we performed time-course long non-coding RNA sequencing (lncRNA-seq) to reveal the gene expression profiles at the early, middle, and late stages of the gallic acid-induced cell death process in human cervical cancer HeLa cells. This work provides a dataset with differentially expressed genes across different stages of cell death process during the gallic acid induction, which is important for further study on the control of this cell death mechanism.
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