Ontology highlight
ABSTRACT:
PROVIDER: PRJNA471227 | ENA |
REPOSITORIES: ENA
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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:To evaluate the DC genome-wide gene expression in response to beta-glucan and its regulation by IL-1 receptor antagonist (IL-1RA) we used a whole genome microarray. The gene expression profiling was performed in DC left untreated or exposed to beta-glucan for 4 and 12 h, in absence or presence of IL-1RA. This strategy allowed the identification of early/immediate and late/secondary genes regulated by beta-glucan in an IL-1-dependent and -independent manner. Human monocyte-derived DC were obtained by a 6/7-d cultures of freshly isolated monocytes with recombinant human IL-4 (10 ng/ml) and GM-CSF (50 ng/ml). Beta-glucan-associated gene expression and its regulation by IL-1RA in human DC was measured in cells left untreated or at 4 and 12 h after exposure to 10 ug/ml of particulate beta-glucan in absence or presence of 2.5 ug/ml of IL-1RA. Five different conditions (Untreated 0h, beta-glucan 4h, IL-1RA + beta-glucan 4h, beta-glucan 12h, and IL-1RA + beta-glucan 12h) were tested using DC from three different donors.
2013-11-01 | E-GEOD-42189 | biostudies-arrayexpress
Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process. Mice receives beta-glucan via ip for 4 days. Splenocytes were isolated for RNA sequencing.
2014-09-26 | E-GEOD-57206 | biostudies-arrayexpress
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.
2021-09-02 | E-MTAB-9982 | biostudies-arrayexpress