E-GEOD-2362
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA91211
PROVIDER: E-GEOD-2362 | ExpressionAtlas | 2014-07-03
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-2362-analysis-methods.tsv | Tabular | |||
| E-GEOD-2362-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-2362-configuration.xml | Xml | |||
| E-GEOD-2362-percentile-ranks.tsv | Tabular | |||
| E-GEOD-2362.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 53 |
Similar Datasets
Project description:Many acquired traits related to fat metabolism are inherited, and nutritional factors can induce fatty liver in chickens. We found that the paternal fatty livers induced by high-fat diet in Jingxing-Huang chickens were inherited, but the molecular mechanisms of inherited fatty liver in chickens are far from clear. The goals of this study are to compare liver transcriptome profiling (RNA-seq) in F1 generation to screen candidate genes for acquired fatty liver. Compared to birds without fatty liver in the control group, the paternal group exhibited altered hepatic gene expression profiles, including up-regulation of several key genes involved in fatty acid metabolism, lipid metabolism and glucose metabolism (ACACA, FASN, SCD, ACSL5, FADS2, FABP1, APOA4 and ME1). This study uniquely revealed that acquired fatty liver in cocks can be inherited. The hepatic gene expression profiles were altered in chickens with the inherited phenotype of acquired paternal fatty liver and several genes could be candidate biomarkers.
2018-04-09 | GSE111909 | GEO
Project description:ARID1A, a DNA-binding component of the SWI/SNF ATP-dependent chromatin-remodeling complex, contributes to nucleosome repositioning and access by transcriptional regulators. Liver-specific deletion of Arid1a (Arid1a LKO) caused the development of age-dependent fatty liver disease in mice. Transcriptome analysis revealed upregulation of lipogenesis and down-regulation of fatty acid oxidation genes.
2019-01-10 | GSE124694 | GEO
Project description:Chronic liver diseases are worldwide on the rise. Due to the rapidly increasing incidence, in particular in Western countries, non-alcoholic fatty liver disease (NAFLD) is gaining importance. As the disease progresses it can develop into hepatocellular carcinoma. Lipid accumulation in hepatocytes has been identified as the characteristic structural change in NAFLD development, but the molecular mechanisms responsible for disease development remained unresolved. Here, we uncover a strong downregulation of the PI3K-AKT pathway and an upregulation of the MAPK pathway in primary hepatocytes from a preclinical model fed with a Western diet (WD). Dynamic pathway modeling of hepatocyte growth factor (HGF) signal transduction combined with global proteomics identifies that an elevated basal MET phosphorylation rate is the main driver of altered signaling leading to increased proliferation of WD-hepatocytes. Model-adaptation to patient-derived hepatocytes reveals a patient-specific variability in basal MET phosphorylation, which correlates with the outcome of patients after liver surgery. Thus, dysregulated basal MET phosphorylation could be an indicator for the health status of the liver and thereby inform on the risk of a patient to suffer from liver failure after surgery.
2024-01-16 | MODEL2306280002 | BioModels
Project description:NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 25895-25901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPARï?¡) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice.
2007-08-31 | E-GEOD-2362 | biostudies-arrayexpress
Project description:Liver-specific deletion of ROCK1 leads to a significant decrease in gene expression of key molecules invovled in lipid systhesis. The study was designed to determine whether hepatic ROCK1 plays a role in the regulation of fatty acid synthesis
2018-12-26 | GSE112548 | GEO
Project description:Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates fatty acid metabolism by positively regulating PPAR-alpha. Hepatocyte-specific deletion of SIRT1 impairs PPAR-alpha signaling and decreased fatty acid beta-oxidation in the liver. When challenged with a high-fat diet, liver-specific SIRT1 knockout mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress. Taken together, our data indicate that SIRT1 plays a vital role in the regulation of hepatic lipid homeostasis.
2009-04-07 | GSE14921 | GEO
Project description:Growth hormone signaling in hepatocytes is fundamentally important. Disruptions in this pathway have led to fatty liver and other metabolic abnormalities. Growth hormone signals through the JAK2/STAT5 pathway. Mice with hepatocyte specific deletion of STAT5 were previously shown to develop fatty liver. Our aim in this study was to determine the effect of deleting JAK2 in hepatocytes on liver gene expression. To do so, we generated animals with hepatocyte specific deletion of JAK2.
2011-05-01 | GSE26188 | GEO
Project description:Melanocortins mediate their biological functions via five different melanocortin receptors (MC1R - MC5R). MC1R is expressed in the skin and leukocytes and is thus involved in the regulation of skin pigmentation and inflammatory responses. MC1R is also present in the liver and white adipose tissue, but its functional role in these tissues is unclear. This study aimed at determining the regulatory role of MC1R in fatty acid metabolism. Recessive yellow (Mc1re/e) mice, a model of global MC1R deficiency, and hepatocyte-specific MC1R deficient mice (Mc1r LKO) were fed a chow or Western diet for 12 weeks. The mouse models were characterized for body weight and composition, adipose tissue mass, adipocyte size, glucose metabolism and lipid metabolism. Furthermore, qPCR and RNA sequencing analyses were used to investigate gene expression profiles in the liver and adipose tissue. HepG2 cells and primary mouse hepatocytes were to study the effects of pharmacological MC1R activation. Chow- and Western diet-fed Mc1re/e showed increased liver weight, white adipose tissue mass and plasma triglyceride (TG) concentration compared to wild type mice. This phenotype occurred without significant changes in food intake, body weight, physical activity or glucose metabolism. Mc1r LKO mice displayed a similar phenotype characterized by larger fat depots, increased adipocyte hypertrophy and enhanced accumulation of TGs in the liver and plasma. In terms of gene expression, markers of de novo lipogenesis, inflammation and apoptosis were upregulated in the liver of Mc1r LKO mice, while enzymes regulating lipolysis were downregulated in white adipose tissue of these mice. In cultured hepatocytes, selective activation of MC1R reduced ChREBP expression, which is a central transcription factor for lipogenesis. Hepatocyte-specific loss of MC1R disturbs fatty acid metabolism in the liver and leads to an obesity phenotype characterized by enhanced adipocyte hypertrophy and TG accumulation in the liver and circulation.
2024-08-29 | GSE262618 | GEO
Project description:In the present study, we explored the hypothesis that the fatty liver phenotype and associated gene expression changes associated with the specific deletion of the POR gene in adult mouse liver could be abrogated by supplementation of the mouse diet with the very long chain highly unsaturated fatty acids, arachidonic acid (C20:4ω6), eicosapentaenoic acid (C20:5ω3) and docosahexaenoic acid (C22:6ω3). We expected the fatty liver phenotype would not be reduced by the polyunsaturated fatty acids linoleic (C18:2ω6) or linolenic acid (C18:3ω3), since these accumulated in the fatty livers of LivPORKO animals. This proved to be the case. However, we also made two surprising observations. First, control animals fed a diet enriched in PUFA had fatty livers and gene expression profiles similar to animals fed a lard diet, which was deficient in both PUFA and HUFA. Second, while a diet enriched in HUFA did result in reduced steatosis in livers of the LivPOKO animals, fat accumulation was still elevated relative to controls. Array analyses indicated most differences in gene expression were related to fatty acid metabolism and could explain differences in fat accumulation in LivPORKO livers with dietary treatment.
2010-10-09 | GSE20944 | GEO
Project description:Growth hormone signaling in hepatocytes is fundamentally important. Disruptions in this pathway have led to fatty liver and other metabolic abnormalities. Growth hormone signals through the JAK2/STAT5 pathway. Mice with hepatocyte specific deletion of STAT5 were previously shown to develop fatty liver. Our aim in this study was to determine the effect of deleting JAK2 in hepatocytes on liver gene expression. To do so, we generated animals with hepatocyte specific deletion of JAK2. Hepatocyte-specific JAK2-deficient mice (JAK2L) were generated by mating floxed JAK2 mice (in a mixed (C57Bl/6:129Sv) background) to mice carrying an Alb promoter-regulated Cre transgene on a 100% C57Bl/6 background purchased from the Jackson Labs. Livers were harvested from 8 week old animals for RNA extraction and hybridization.
2011-04-30 | E-GEOD-26188 | biostudies-arrayexpress