Project description:Methods: RNA transcription profiling of intrahepatic CD4-CD8- double negative T cells were compared between C57BL/6 mice fed with control diet and methionine-choline deficient diet (MCD) for 5 weeks. Results: RNA sequencing data showed that intrahepatic DNT in NAFLD mice exhibited markedly decreased Prf1, Gzmb but increased Il17a expression.
Project description:Phosphatidylcholine transfer protein (PC-TP, a.k.a StarD2) is abundantly expressed in liver and is regulated by PPARα. When fed the synthetic PPARα ligand fenofibrate, Pctp-/- mice exhibited altered lipid and glucose homeostasis. Microarray profiling of liver from fenofibrate fed wild type and Pctp-/- mice revealed differential expression of a broad array of metabolic genes, as well as their regulatory transcription factors. Because its expression controlled the transcriptional activities of both PPARα and HNF4α in cell culture, the broader impact of PC-TP on nutrient metabolism is most likely secondary to its role in fatty acid metabolism. 6 livers collected from PC-TP knockout mice fed a fenobrate-supplemented diet were used as the experimental group. 6 livers collected from wild type mice fed a fenofibrate-supplemented diet were used as the control group. RNA prepared from one liver was used to hybridize one GeneChip, so that there were 6 experimental GeneChips and 6 control GeneChips.
Project description:Transcriptional profiling of adult mouse liver tissue comparing offspring derived from sperm and seminal plasma of normal protein diet fed males (controls, NN), sperm and seminal plasma from males fed a low protein diet fed males (LL), sperm from normal protein fed males and seminal plasma from low protein fed males (NL) or sperm from low protein diet fed males and seminal plasma from normal protein diet males (NL). The first letter denotes the diet of the sperm donor and the second letter the diet of the seminal plasma donor. Three-condition experiment: NN vs. LL, NN vs. NL, NN vs. LN. Adult offspring liver tissue. Biological replicates: 7 control (NN), 9 LL, 7 NL and 7 LN. One replicate per array chip.
Project description:The conserved phosphoprotein MAF1 is the main known direct repressor of RNA polymerase III (Pol III). MAF1 is phosphorylated and inactivated by the nutrient-sensing TORC1 kinase, making MAF1 a nutrient effector for Pol III transcription. MAF1 has been associated with lipid metabolism in D. melanogaster, C. elegans, and the mouse. However, whereas downregulation of Maf1 generally increases lipogenesis, Maf1-/- mice are lean even under a High Fat (HF) diet. Here we compared Maf1-/- mice fed a Chow diet with mice lacking Maf1 specifically in hepatocytes (Maf1hep-/- mice) fed either a Chow or HF diet. Unlike Maf1-/- mice, Maf1hep-/- mice become slightly heavier than control mice at an old age and much earlier under a HF diet, with increased adiposity. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and subtle changes in protein accumulation that are consistent with increased lipogenesis. RNAseq and metabolite profiling indicate that liver phenotypes of Maf1-/- mice are strongly influenced by systemic inter-organ communication. Notable changes observed in the three phenotypically distinct cohorts include downregulation of Mouse Urinary Proteins, upregulation of Cyp2a4 expression, suggestive of an alteration of Growth Hormone levels or secretion pattern, and downregulation of Angiogenin, a phenomenon that might be directly linked to increased Pol III occupancy of tRNA genes in the main Angiogenin promoter region.
Project description:Microarray analysis showed dysregulation of genes involved in lipid, xenobiotic and glutathione metabolism as well as those involved in mitochondrial function and cell proliferation in the livers of C57BL6 mice fed alcoholic liquid diet for 6 weeks. We analyzed liver RNA from 4 mice fed alcoholic diet and 4 mice fed control diet using the Affymetrix Mouse Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool.
Project description:Germ free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice. CARB-fed indicates a standard polysaccharide-rich mouse chow diet. CONV-D mice are those that received a microbiota transplant from conventionally raised mice 2-3 weeks before experiment was initiated Keywords: RNA Expression Array
Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent, bio-accumulative pollutant that has been used for the last 60+ years in numerous industrial and commercial applications. In mice, PFOS administration is known to induce hepatomegaly and hepatic steatosis. The aim of the present study was to evaluate potential PFOS and diet interactions and explore the mechanism of PFOS induced liver lipid accumulation. Prior to PFOS administration, mice were fed either a standard chow diet (SD) or 60% kCal high fat diet (HFD) for 4 weeks to establish significant body weight increase. After 4 weeks of diet acclimation, the treatment groups received 0.0003% PFOS in diet for an additional 10 weeks. In addition, a subset of the mice fed HFD were switched to a SD (H-SD) to mimic weight-loss induced improvement of hepatic steatosis. A total of six treatment groups: i) SD, ii) HSD, iii) HFD (H), iv) SD +PFOS(SDP), v) H-SD +PFOS (HSDP), and vi) HFD +PFOS (HP) were included. PFOS and lipid concentrations were measured in both serum and liver. Relative liver mRNA expression was determined by targeted bead array and proteins were quantified using untargeted mass spectrometry. PFOS exposure increased liver weight, and in the HFD increased liver triglycerides and liver cholesterol content. Gene and protein expression in the liver demonstrated that PFOS exposure induced lipid utilization and xenobiotic metabolism pathways, and in a HFD, induced lipid synthesis. The data suggests that PFOS exposure acts on lipid utilization genes and exacerbates hepatic steatosis in mice fed a HFD.
Project description:To identify molecular mechanism underlying the protection from diet-induced hepatic steatosis in AHNAK deficiency mice, we examined microarray analysis with liver sample from HFD-fed AHNAK KO and WT mice. Two-condition experiment, regular chow (CD) -fed WT vs. CD-fed AHNAK KO and High fat diet(HFD)-fed WT vs. HFD-fed AHNAK KO mice. Biological replicates: 3 control, One replicate per array.
Project description:To profile the expression of circulating miRNAs in a mouse model of diet-induced obesity (DIO) with subsequent weight-reduction with low-fat diet (LFD), eighteen C57BL/6 male mice were grouped into three subgroups as: (1) Control: the mice fed with the standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice fed with 58 kcal% high-fat diet for 12 wks; (3) DIO+LFD: the mice fed with high-fat diet for 8 wks to induce obesity, then changed to 10.5 kcal% low-fat diet for subsequent 4 wks.