Project description:Comparison of liver transcriptome between RC-fed mice, HFD-fed mice with vehicle or nobiletin treatment provides the possibility to identify the effects of nobiletin on gene expression altered by HFD relative to RC. We used Illumina microarrays to analyze liver transcriptome of different treatment groups following exposure to RC, HFD.Veh (denoted as the HFD group) and HFD.NOB (denoted as the NOB group). The microarray experiment was performed to investigate effects of HFD and NOB on mouse liver transcriptome. Liver tissues were collected at ZT2 and ZT14 (corresponding to 2 hours after light on and light off, respectively). The pooled RNA samples, 4 mice each group, were used for the microarray.
Project description:Proteomics of liver tissue from mice fed a high fat diet (HFD) or regular chow diet. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021
Project description:To investigate the effect of diet and Yap KD on liver matastasis, we injected MC38 cells in LFD-fed or HFD-fed mice, and MC38 with shCon or shRNA for Yap (shYap1) in HFD-fed mice We then performed gene expression profiling analysis using data obtained from RNA-seq of these 4 different conditions
Project description:Comparison of liver transcriptome between RC-fed mice, HFD-fed mice with vehicle or nobiletin treatment provides the possibility to identify the effects of nobiletin on gene expression altered by HFD relative to RC. We used Illumina microarrays to analyze liver transcriptome of different treatment groups following exposure to RC, HFD.Veh (denoted as the HFD group) and HFD.NOB (denoted as the NOB group).
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.
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of wild-type C57BL-6 mice exposed to a high-fat diet that might have been caused by the oral consumption of the probiotic B. pseudocatenulatum CECT 7765. The aim of this work was to determine whether the daily intake (by oral gavage) of the probiotic (P) B. pseudocatenulatum for seven weeks exerted any modulatory effects, at the level of gene expression, in the liver of C57BL-6 male mice exposed to a high-fat diet (HFD). Male mice were randomly assigned to four experimental groups (n= 5 animals per group) as follows: (1) control group, fed a standard diet (SD); (2) obese group, fed a high-fat diet (HFD); (3) a group that received the SD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (SD+P); and (d) an obese group that was fed the HFD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (HFD+P). At the end of the experimental procedure total RNA was extracted from the liver to compare differential gene expression between the groups. Liver differential gene expression after 7 weeks of supplementation between: 1) the HFD group and the SD group (effects of the high-fat diet); 2) the HFD+P and the HFD (effects of the probiotic on the consumption of a high-fat diet) and 3) the SD+P group and the SD (direct effects of the probiotic on the liver of animals consuming a normal diet).
Project description:To understand the fibrotic response in the CDA-HFD induced NASH fibrosis model, we performed RNA-seq on liver samples collected from mice fed with normal chow (week 0) or CDA-HFD chow (weeks 8 and 16).