Ontology highlight
ABSTRACT:
PROVIDER: PRJNA787736 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17221855_1.fastq.gz | Fastqsanger.gz | |||
| SRR17221855_2.fastq.gz | Fastqsanger.gz | |||
| SRR17221856_1.fastq.gz | Fastqsanger.gz | |||
| SRR17221856_2.fastq.gz | Fastqsanger.gz | |||
| SRR17221857_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 70 |
Similar Datasets
Project description:FLORINASH - The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) EU FP7-HEALTH, project number 241913<br>Florinash examined the role on the gut microbiota in NAFLD. Metagenomic, proteomic, metabolomic and transcriptomic data were integrated to give provide a systems biology approach to disease-associated studies. Liver biopsies were obtained from patients undergoing bariatric surgery; one was used to diagnose NAFLD, the other was used to examine the host transcriptome in NAFLD. This dataset is part of the TransQST collection.
2018-03-15 | E-MTAB-4856 | biostudies-arrayexpress
Project description:Lean nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a distinct clinical phenotype with limited evidence for effective non-pharmacological interventions and unclear mechanistic pathways. Aerobic exercise is recommended for NAFLD management, yet its effects and underlying gut microbiota–mediated mechanisms in lean NAFLD remain insufficiently characterized. This study is based on a randomized controlled trial (ClinicalTrials.gov identifier: NCT04882644) in which 100 adults with lean NAFLD were randomly assigned to a 3-month aerobic exercise intervention or usual care. 63 paired fecal samples were collected at baseline and after intervention. Gut microbiota profiles were generated using 16S rRNA gene sequencing. The dataset includes processed taxonomic abundance tables derived from fecal samples collected before and after the intervention. These data were used to characterize exercise-induced alterations in gut microbial diversity, composition, and functional potential, and to explore interindividual heterogeneity in microbiota responses to aerobic exercise in lean NAFLD. The microbiome data deposited in this series support integrative analyses with clinical phenotypes and circulating metabolomic profiles, aiming to elucidate gut microbiota–associated mechanisms underlying the metabolic benefits of aerobic exercise in lean NAFLD.
2025-12-18 | GSE314066 | GEO
Project description:Background & Aims: Non-alcoholic fatty liver disease (NALFLD)-associated changes in gut microbiota are important drivers of disease progression toward fibrosis. Therefore, reversing microbiota alterations could ameliorate NAFLD progression. Oat beta-glucan, a non-digestible polysaccharides, has shown promising therapeutic effects on hyperlipidemia associated with NAFLD, but its impact on gut microbiota and most importantly NAFLD fibrosis remains unknown. Methods: We performed detailed metabolic phenotyping including body composition, glucose tolerance, and lipid metabolism as well as comprehensive characterization of the gut-liver axis in a western-style diet (WSD)-induced model of NAFLD and assessed the effect of a beta-glucan intervention on early and advanced liver disease. Gut microbiota was modulated using broad-spectrum antibiotic (Abx) treatment. Results: Oat beta-glucan supplementation did not affect WSD-induced body weight gain, glucose intolerance, and the metabolic phenotype remained largely unaffected. Interestingly, oat beta-glucan dampened NAFLD inflammation, associated with significantly reduced monocyte-derived macrophages (MoMFs) infiltration, fibroinflammatory gene expression, and strongly reduced fibrosis development. Mechanistically, this protective effect was not mediated by changes in bile acid composition or signaling, but was dependent on gut microbiota and was lost upon Abx treatment. Specifically, oat beta-glucan partially reversed unfavorable changes in gut microbiota, resulting in an expansion of protective taxa, including Ruminococcus, and Lactobacillus followed by reduced translocation of TLR ligands. Conclusions: Our findings identify oat beta-glucan as a highly efficacious food supplement that dampens inflammation and fibrosis development in diet-induced NAFLD. These results, along with its favorable dietary profile, suggest that it may be a cost-effective and well-tolerated approach to preventing NAFLD progression and should be assessed in clinical studies.
2024-01-01 | GSE246738 | GEO
Project description:Lean nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a distinct clinical phenotype with limited evidence for effective non-pharmacological interventions and unclear mechanistic pathways. Aerobic exercise is recommended for NAFLD management; however, its effects and the gut microbiota–associated mechanisms in lean NAFLD remain incompletely understood. This dataset was generated from a randomized controlled trial (ClinicalTrials.gov identifier: NCT04882644). Participants assigned to the aerobic exercise intervention group provided fecal samples at baseline and after the 3-month intervention. A total of 33 paired fecal samples were included in this dataset. Gut microbiota profiles were generated using shotgun metagenomic sequencing. The dataset includes processed and de-identified species-level relative abundance tables derived from fecal samples collected before and after the intervention. These data were used to characterize exercise-induced alterations in gut microbial composition and interindividual variability in microbiota responses to aerobic exercise in lean NAFLD. The data support integrative analyses with clinical phenotypes and circulating metabolomic profiles to explore gut microbiota–associated mechanisms underlying the metabolic benefits of aerobic exercise.
2025-12-23 | GSE314617 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming the most common liver disease worldwide, yet the pathogenesis of NAFLD is only partially understood. Here, we investigated the role of the gut bacteria in NAFLD by stimulating the gut bacteria via feeding mice the fermentable dietary fiber guar gum and suppressing the gut bacteria via chronic oral administration of antibiotics. Guar gum feeding profoundly altered the gut microbiota composition, in parallel with reduced diet-induced obesity and improved glucose tolerance. Strikingly, despite reducing adipose tissue mass and inflammation, guar gum enhanced hepatic inflammation and fibrosis, concurrent with markedly elevated plasma and hepatic bile acid levels. Consistent with a role of elevated bile acids in the liver phenotype, treatment of mice with taurocholic acid stimulated hepatic inflammation and fibrosis. In contrast to guar gum, chronic oral administration of antibiotics effectively suppressed the gut bacteria, decreased portal secondary bile acid levels, and attenuated hepatic inflammation and fibrosis. Neither guar gum or antibiotics influenced plasma lipopolysaccharide levels. In conclusion, our data indicate a causal link between changes in gut microbiota and hepatic inflammation and fibrosis in a mouse model of NAFLD, possibly via alterations in bile acids.
2017-06-06 | GSE76087 | GEO
Project description:Periodontitis increases the risk of non-alcoholic fatty liver disease (NAFLD). However, the precise mechanisms are unclear. Here, gut dysbiosis induced by orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, was implicated in the deterioration of NAFLD pathology. C57BL/6 mice were administered with the vehicle, P. gingivalis or Prevotella intermedia, with weaker periodontal pathogenicity, followed by feeding on a choline-deficient, high fat diet (CDAHFD60). CDAHFD60 feeding induced hepatic steatosis, and combined bacterial administration further aggravated NAFLD pathology with increased fibrosis. Liver gene expression analyses revealed that genes involved in the NAFLD pathology were perturbed with distinctive expression profiles induced by different bacteria. These differences may be due to quantitative and qualitative differences in the influx of gut bacterial products because the serum endotoxin level, gut microbiota composition, and serum metabolite profile caused by ingested P. intermedia and P. gingivalis were different. These findings provide insights into mechanisms linking periodontitis and NAFLD.
2021-11-03 | GSE136937 | GEO
Project description:MaternalWestern-style diet (WD) disrupts early life gut microbiota in the offspring and is associated with pediatric nonalcoholic fatty liver disease (NAFLD). Here, we report that oral supplementation with gut-derived tryptophan metabolites indole (Ind) or indole-3-acetate (I3A) during pregnancy and lactation in WD-fed dams had persistent effects in offspring liver, acting on key upstream regulators in WD-challenged offspring that suppress pathways for steatosis, fibrosis, and oxidative stress. Maternal Ind or I3A activated aryl hydrocarbon receptor (AHR) signaling, leading to increases in long-chain and very long-chain (VLC) ceramides in offspring liver and small intestine. These effects were evident as early as postnatal day 14. The tryptophan metabolite 5-hydroxyindoleacetate (5-HIAA), an AHR ligand, was depleted in offspring by maternal WD and restored by maternal I3A treatment. Fecal transplantation studies demonstrated that VLC ceramides and liver fibrosis remodeling were mediated by maternal indoles altering the gut microbiota, with strong associations with Lactobacillaceae. Collectively, these findings define a novel and persistent protective effect of maternal Ind and I3A to prevent NAFLD, acting both directly on the liver and through the microbiota. These tryptophan metabolites may serve as therapeutic targets for future interventional studies aimed at prevention of pediatric NAFLD.
2026-01-21 | GSE247323 | GEO
Project description:Those FASTQ are used in a paper where are primarily compared the variations in the oral microbiota composition between HIV patients and healthy controls (HC). In addition, it is performed a longitudinal evaluation of the oral-gut microbiota-immunity axis from HIV-infected patients before starting ART (T0) and after reaching virological suppression (T24 weeks).
2025-09-01 | GSE242855 | GEO
Project description:Gut microbiota alternations by PED infection
| PRJEB8875 | ENA