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Gene expression profile at single cell level of liver non-parenchymal cells (NPC) from mice with or without high fat diet (HFD) and physical exercise interventions

ABSTRACT: Exercise is pivotal for the prevention and treatment of non-alcoholic fatty liver disease (NAFLD). We used single-cell RNA sequencing (scRNA-seq) to analyse the diversity and intricacies of multiple cellular and molecular responses in the liver of mice with HFD-induced NAFLD and exercise interventions, and revealed a previously underappreciated role of hepatic immune cells in mediating the beneficial effects of exercise

ORGANISM(S): Mus musculus

PROVIDER: GSE252248 | GEO | 2026/05/20

REPOSITORIES: GEO

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RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice

Project description:RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice

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Comparison of miRNA expression profile among the livers of C57BL/6J control mice, high fat diet (HFD) mice and metformin treated mice

Project description:Nonalcoholic fatty liver disease (NAFLD) is a growing worldwide epidemic and an important risk factor for the development of insulin resistance, type 2 diabetes, nonalcoholic steatohepatitis (NASH), and hepatic cellular carcinoma (HCC). Despite the prevalence of NAFLD, lifestyle interventions involving exercise and weight loss are the only accepted treatments for this disease. Over the past years, metformin has been shown to improve NAFLD in preclinical animal models. Hepatic microRNAs (miRNAs) have been suggested as therapeutic targets because of their involvement in the progression of NAFLD. The aim of this study was to identify miRNAs associated with the regulation of liver lipid metabolism after metformin treatment. We performed computational analysis of the function enrichment and disease association of the differentially expressed miRNAs and their targets. Our analysis may shed light on the novel treatment method for NAFLD.

2018-06-21 | GSE94799 | GEO

Comparison of circRNA expression profile among the livers of C57BL/6J control mice, high fat diet (HFD) mice and metformin treated mice

Project description:Nonalcoholic fatty liver disease (NAFLD) is a growing worldwide epidemic and an important risk factor for the development of insulin resistance, type 2 diabetes, nonalcoholic steatohepatitis (NASH), and hepatic cellular carcinoma (HCC). Despite the prevalence of NAFLD, lifestyle interventions involving exercise and weight loss are the only accepted treatments for this disease. Over the past years, metformin has been shown to improve NAFLD in preclinical animal models. Several coding and non-coding genes have been suggested to contribute to the metformin treatment mechanism of NAFLD. Circulating RNA (circRNA) is a novel group of non-coding RNAs which may have regulatory role in vivo. This study firstly probe the potential role of circRNA in the treatment of NAFLD by the microarray circRNA expression profiling.

2018-06-21 | GSE94841 | GEO

Comparison of lncRNA and mRNA expression profile among the livers of C57BL/6J control mice, high fat diet (HFD) mice and metformin treated mice

Project description:Nonalcoholic fatty liver disease (NAFLD) is a growing worldwide epidemic and an important risk factor for the development of insulin resistance, type 2 diabetes, nonalcoholic steatohepatitis (NASH), and hepatic cellular carcinoma (HCC). Despite the prevalence of NAFLD, lifestyle interventions involving exercise and weight loss are the only accepted treatments for this disease. Over the past years, metformin has been shown to improve NAFLD in preclinical animal models. However, whether and how the long non-coding RNAs (lncRNAs) were involved in the progression of NAFLD and the mechanism of metformin treatment were not clearly understood. The aim of this study was to identify lncRNAs associated with the regulation of liver lipid metabolism after metformin treatment. We performed computational analysis of the function enrichment of the differentially expressed lncRNAs and mRNAs. Our analysis also suggested significant co-expression between hepatic lncRNAs and their predicted mRNA targets. Our analysis suggests a noticeable role in the etiology and treatment of NAFLD.

2018-06-21 | GSE94790 | GEO

microRNA data from high-fat diet fed mice with and without exercise

Project description:Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle. Exercise is known to be beneficial for NAFLD treatment. Recent studies have shown the critical involvement of microRNA in NAFLD. However, it is unclear whether exercise could prevent NAFLD via miRNA targeting. We used microarrays to examine microRNA profiles in high-fat diet fed mice with and without exercise in comparison to normal diet fed mice.

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Cdo1-Camkk2-AMPK axis confers the protective effects of exercise against NAFLD in mice

Project description:Cysteine dioxygenase type 1 (Cdo1) is a key enzyme for cysteine catabolism that is enriched in liver, whose role in NAFLD remains poorly understood. Here, we show that exercise induces the expression of hepatic Cdo1 via the cAMP/PKA/CREB signaling pathway. Hepatocyte-specific knockout of Cdo1 (Cdo1LKO) impairs the effect of exercise against NAFLD, whereas hepatocyte-specific overexpression of Cdo1 (Cdo1LTG) and exercise synergistically ameliorates NAFLD in male mice. Mechanistically, Cdo1 facilitates the binding between AMPK and kinase active Camkk2, which activates AMPK signaling. This promotes fatty acid oxidation and mitochondrial biogenesis in hepatocytes to attenuate hepatosteatosis. Therefore, by promoting hepatic Camkk2-AMPK signaling pathway, Cdo1 acts as an important downstream effector of exercise to combat against NAFLD

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RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice

Project description:RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice

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Genome-wide liver transcriptomic profiles from chow-fed, high fat diet (HFD) fed, and HFD + AC261066 (Retinoic Acid Receptor Beta-2 Selective Agonist) fed mice

Project description:Using a high fat diet (HFD) mouse model of nonalcoholic fatty liver disease (NAFLD) with 60% of the energy derived from fat, we determined the effects of AC261066, a RARbeta2 selective agonist, on the liver transcriptome. We analyzed disease signature pathways using our genome-wide RNA-seq data from AC260166 treated livers and show that AC261066 limits the mRNA increases of NAFLD driver genes PKLR, FASN, THRSP, and CHCHD6. Moreover, AC261066’s effects on the hepatic stellate cell (HSC) secretome signature and changes in other transcripts that contribute to fibrosis suggest that AC261066 suppresses the initiation of liver fibrosis, which characterizes NASH. Our RNA-seq data also indicate an anti-inflammatory effect of AC261066. In conclusion, based on our genome-wide analysis of the transcriptome of NAFLD, we suggest that AC261066 has potential therapeutic relevance for the prevention/treatment of NAFLD and NASH.

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miRNA seq mouse liver HFD, PCB126, Aroclor1260 exposure

Project description:Exposure to high fat diet (HFD) and persistent organic pollutants including polychlorinated biphenyls (PCBs) is associated with liver injury in human populations and with non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in animal models. Exposure of HFD-fed male mice to the non-dioxin-like (NDL) PCB mixture Aroclor1260 or to dioxin-like (DL) PCB126 or to the combination caused steatohepatitis and differentially altered the liver proteome with pathways involving epigenetic regulation of gene expression. Here unbiased RNA sequencing of miRNA (miRNA-seq) and subsequent network analysis to characterize the biological pathways altered by HFD and PCB exposure compared to HFD alone. Distinct miRNA expression patterns reveald a potential role of miRNAs in the pathogenesis of NAFLD. These results demonstrate miRNA and transcriptome pathways in PCB-related hepatic inflammation and fibrosis in a mouse model of NAFLD.

2024-04-23 | GSE195829 | GEO

16S rRNA gene sequencing of human fecal microbiota before and after exercise intervention

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