Ontology highlight
ABSTRACT:
PROVIDER: PRJNA737039 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14793100_1.fastq.gz | Fastqsanger.gz | |||
| SRR14793100_2.fastq.gz | Fastqsanger.gz | |||
| SRR14793101_1.fastq.gz | Fastqsanger.gz | |||
| SRR14793101_2.fastq.gz | Fastqsanger.gz | |||
| SRR14793102_1.fastq.gz | Fastqsanger.gz |
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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:Non alcoholic fatty liver disease (MASLD) is a multifactorial disease, and the imbalance of gut microbiota is closely related to its occurrence and development. Traditional Chinese Medicine (TCM) constitution theory holds that differences in constitution affect the development of diseases. This study aims to explore the compositional changes of fecal microbiota in MASLD patients with different constitutions, in order to provide new insights into the molecular mechanisms of MASLD.
2025-08-18 | PXD067450 |
Project description:Mardinoglu2014 - Genome-scale metabolic model
(HMR version 2.0) - human hepatocytes (iHepatocytes2322)
This model is described in the article:
Genome-scale metabolic
modelling of hepatocytes reveals serine deficiency in patients
with non-alcoholic fatty liver disease.
Mardinoglu A, Agren R, Kampf C,
Asplund A, Uhlen M, Nielsen J.
Nat Commun 2014; 5: 3083
Abstract:
Several liver disorders result from perturbations in the
metabolism of hepatocytes, and their underlying mechanisms can
be outlined through the use of genome-scale metabolic models
(GEMs). Here we reconstruct a consensus GEM for hepatocytes,
which we call iHepatocytes2322, that extends previous models by
including an extensive description of lipid metabolism. We
build iHepatocytes2322 using Human Metabolic Reaction 2.0
database and proteomics data in Human Protein Atlas, which
experimentally validates the incorporated reactions. The
reconstruction process enables improved annotation of the
proteomics data using the network centric view of
iHepatocytes2322. We then use iHepatocytes2322 to analyse
transcriptomics data obtained from patients with non-alcoholic
fatty liver disease. We show that blood concentrations of
chondroitin and heparan sulphates are suitable for diagnosing
non-alcoholic steatohepatitis and for the staging of
non-alcoholic fatty liver disease. Furthermore, we observe
serine deficiency in patients with NASH and identify PSPH,
SHMT1 and BCAT1 as potential therapeutic targets for the
treatment of non-alcoholic steatohepatitis.
This model is hosted on
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and identified by:
MODEL1402200003.
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2005-01-01 | MODEL1402200003 | BioModels
Project description:Non–alcoholic fatty liver disease (NAFLD) is high prevalent in worldwide and associated with chronic kidney disease (CKD). Infection with Opisthorchis viverrini (Ov) infection and consumption of high fat and high fructose (HFF) exacerbates NAFLD to nonalcoholic steatohepatitis in hamsters. Here, we aimed to investigate the effect a combination of HFF diet and Ov infection on kidney pathology via alteration of gut microbiome and proteome in hamster.
2024-09-12 | PXD045309 | JPOST Repository
Project description:Neutrophils in Non-alcoholic fatty liver disease
| PRJNA1070345 | ENA
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