Ontology highlight
ABSTRACT:
PROVIDER: PRJNA812677 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18216817_1.fastq.gz | Fastqsanger.gz | |||
| SRR18216817_2.fastq.gz | Fastqsanger.gz | |||
| SRR18216818_1.fastq.gz | Fastqsanger.gz | |||
| SRR18216818_2.fastq.gz | Fastqsanger.gz | |||
| SRR18216819_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 42 |
Similar Datasets
Project description:Recent studies have revealed the pivotal role of gut microbiota in the precession of liver diseases including non-alcoholic steatohepatitis (NASH). Many natural herbs, such as Gynostemma pentaphyllum (GP), have been extensively used applied in the treatment prevention of NASH, while the bioactive components and underlying mechanism remain unclear. The aim of this study was to investigate whether the polysaccharides of GP (GPP) has the protective effect on of NASH and to explore the potential mechanism underlying these effects. To investigate the function high dose of GPP(HGPP) in the regulation of hepatic gene expression, C57BL/6 male mice were fed with methionine-choline-deficient (MCD) diet for 4 weeks to induce NASH, and administered daily oral gavage of the sodium carboxymethylcellulose (CMC-Na) for model group, HGPP for experimental group, compared with normal control methionine-choline-sufficient (MCS) group.
2022-06-16 | GSE205974 | GEO
Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.
2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress
Project description:Kupffer cells (KCs) self-renew by local proliferation in the adult independently from monocytes (Mos). However, how they maintain during chronic metabolic disorders such as non-alcoholic steatohepatitis (NASH) remains ill-defined. We characterized KCs during NASH and observed diversity in the KC pool, with a significant fraction of monocyte-derived KCs (MoKCs). Here, we aim to uncover the transcriptional landscapes of KCs subsets found in a mouse model of methionine and choline deficient (MCD)-diet induced non-alcoholic steatohepatitis (NASH).
2020-12-04 | GSE138778 | GEO
Project description:Lipid accumulation associated with immune cell infiltration leading to hepatocellular ballooning and lobular inflammation are the cardinal features of NASH. With onset and development of multi-omics approaches in the last decade, we have been able to comprehend the existence and functionality of gut microbial ecology. Apart from the compositional variation (dysbiosis), functional alteration of the microbial population i.e., the impact of the crosstalk between gut microbiota-derived metabolites with host cells also remains elusive in terms of regulation of immunometabolic homeostasis and overall human health and disease. Sodium butyrate (NaBu), a short chain fatty acid derived metabolite is known to modulate the inflammatory status of NASH pathogenesis; however, its mechanism of action is not clearly deciphered. To unveil the immunomodulatory activity of NaBu, we found robust anti-inflammatory effect of NaBu in diet induced NASH model with reduced macrophage infiltration. Mechanistically, independent of p65 nuclear translocation, by maintaining the enhanced acetylation status of p65 along with differential p65 recruitment to the proinflammatory gene promoter, NaBu suppressed the inflammatory milieu and resulted in better prognosis. Along with transcriptional rewiring, NaBu also altered the metabolic status, modified the functional outcome and exhibited differential secretome which ultimately resulted skewing of macrophages towards a prohealing phenotype and induced autocrine as well as paracrine death of proinflammatory macrophages to abrogate inflammation in both isolated LMs and in vivo model.
2023-01-15 | GSE219093 | GEO
Project description:Purpose: The goals of this study is to use NGS-derived liver transcriptome profiling (RNA-seq) to identify candidates of pathways and genes which are responsible to protect MttpIKO from MCD induced-NASH development .
2021-10-20 | GSE182130 | GEO
Project description:We fed control mice and Slc7a11-LTG mice methionine and Choline Deficient (MCD) to induce NASH. Whole-genome RNA sequencing were then performed in the livers of control and LTG mice fed with MCD.
2025-09-09 | GSE213182 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries. There is growing evidence that dysbiosis of the intestinal microbiota and disruption of microbiota-host interactions contribute to the pathology of NAFLD. We previously demonstrated that gut microbiota derived tryptophan metabolite indole-3-acetate (I3A) was decreased in both cecum and liver of high-fat diet-fed mice and attenuated the expression of inflammatory cytokines in macrophages and TNF-a and fatty acid induced inflammatory responses in an aryl-hydrocarbon receptor (AhR) dependent manner in hepatocytes. In this study, we investigated the effect of orally administered I3A in a mouse model of diet induced NAFLD. Western diet (WD)-fed mice given sugar water (SW) with I3A showed dramatically decreased serum ALT, hepatic TG, liver steatosis, hepatocyte ballooning, lobular inflammation, and hepatic production of inflammatory cytokines, compared to WD-fed mice given only SW. Metagenomic analysis show that I3A administration did not significantly modify the intestinal microbiome, suggesting that I3A’s beneficial effects likely reflect the metabolite’s direct actions on the liver. Administration of I3A partially reversed WD induced alterations of liver metabolome and proteome, notably, decreasing expression of several enzymes in hepatic lipogenesis and β- oxidation. Mechanistically, we also show that AMP-activated protein kinase (AMPK) mediates the anti-inflammatory effects of I3A in macrophages. The potency of I3A in alleviating liver steatosis and inflammation clearly demonstrates its potential as a therapeutic modality for preventing the progression of steatosis to NASH.
2024-02-23 | PXD046255 | Pride
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
2024-03-20 | GSE261887 | GEO