Hepatic gene expression profiles of db/db mice with non-alcoholic fatty liver
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA422882 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Nonalcoholic fatty liver disease (NAFLD) is a common disorder in obese people and is becoming the leading cause of hepatocellular carcinoma (HCC). Recently, lncRNAs have been proven to play remarkable roles in numerous biological processes and human diseases, including NAFLD. However, the function of lncRNA in NAFLD pathogenesis remains largely unknown. The aim of this study was to explore the lncRNA expression profile in NAFLD mice and to identify novel lncRNAs involved in the pathogenesis of NAFLD. We performed microarray analysis to compare the expression profiles of lncRNAs and mRNAs in the liver of diabetic db/db mice with NAFLD and normal mice.
2017-12-19 | GSE108228 | GEO
Project description:Major causes of lipid accumulation in liver are increased import, synthesis or decreased catabolism of fatty acids. The latter is caused by dysfunction of cellular organelle controlling energy homeostasis, i.e. mitochondria. However, peroxisomes appear to be an important organelle in lipid metabolism of hepatocytes, but little is known about their role in the development of non-alcoholic fatty liver disease (NAFLD). To investigate the role of peroxisomes next to mitochondria in excessive hepatic lipid accumulation we used the leptin resistant db/db mice on C57BLKS background, a mouse model that develops hyperphagia induced diabetes with obesity and NAFLD. We used microarrays to determine differences in hepatic gene expression in a mouse model for NAFDL (BKS.Cg-Leprdb (db/db)) and their wildtype littermates C57BL/KSlepr+/+ (BKS) to determine the effect of persistent hepatic lipid accumulation.
2015-03-23 | GSE59930 | GEO
Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes. There are 12 samples in our study which belonged to 4 groups, and each group contains 3 different samples.
2015-01-23 | E-GEOD-65220 | biostudies-arrayexpress
Project description:Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to hepatic macrophages in high-fat diet -induced non-alcoholic fatty liver disease. Methods and results: Wild-type and Casp11-/- mice were treated with high fat and normal chow diet for a period of 12 weeks. Hepatic macrophages from liver were isolated to generate mRNA transcription. Conclusion: Our study represents detailed analysis of caspase-11 in regulating hepatic macrophages in high-fat diet -induced non-alcoholic fatty liver disease.
2023-01-17 | GSE221005 | GEO
Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes.
2015-01-23 | GSE65220 | GEO
Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis. Human liver samples of steatosis and non-alcoholic steatohepatitis were selected for RNA extraction and hybridization on Affymetrix microarrays. This dataset is part of the TransQST collection.
2014-11-07 | E-GEOD-63067 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease worldwide and is estimated to affect nearly a third of the population. Huwe1, also known as ARF-BP1, MULE, and HectH9, is a HECT (homology to E6-APC terminus)-domain E3 ubiquitin ligase originally identified as a binding partner of the tumor suppressor ARF, as well as a direct negative regulator of the tumor suppressor p53. To further elucidate the in vivo role of Huwe1, we generated a liver-specific Huwe1 (Huwe1LKO) knockout mouse model. Surprisingly, liver-specific knockout of Huwe1 protected mice from the development of age-induced hepatic steatosis. To elucidate the mechanism underlying this phenotype, mass spectrometry analysis was performed on liver tissues from 1-year-old Huwe1LKO and Huwe1WT mice.
2024-01-26 | PXD045279 | Pride
Project description:In this study, we explored the role of macrophage scavenger receptor 1 (MSR1) in the progression of non-alcoholic fatty liver disease. Mice lacking Msr1 proved to be protected against high fat-cholesterol diet (HFD)-induced metabolic disorder, showing fewer hepatic lipid-laden foamy macrophages, less hepatic inflammation and changed lipid metabolism.
2022-02-01 | GSE163471 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease worldwide and is estimated to affect nearly a third of the population. Huwe1, also known as ARF-BP1, MULE, and HectH9, is a HECT (homology to E6-APC terminus)-domain E3 ubiquitin ligase originally identified as a binding partner of the tumor suppressor ARF, as well as a direct negative regulator of the tumor suppressor p53. To further elucidate the in vivo role of Huwe1, we generated a liver-specific Huwe1 (Huwe1LKO) knockout mouse model. Surprisingly, liver-specific knockout of Huwe1 protected mice from the development of age-induced hepatic steatosis. To elucidate the mechanism underlying this phenotype, bulk RNAseq analysis was performed on liver tissues from 1-year-old Huwe1LKO and Huwe1WTmice.
2023-12-06 | GSE241875 | GEO
Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis.
2014-11-07 | GSE63067 | GEO