Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of liver from PPARalpha knockout mice: PPARa -dependent regulation of hepatic lipid metabolism by expression profiling (GEO Super series)

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE8290: Comprehensive analysis of PPARÎ±-dependent regulation of hepatic lipid metabolism by expression profiling - 1; GSE8291: Comprehensive analysis of PPARÎ±-dependent regulation of hepatic lipid metabolism by expression profiling - 2; GSE8292: Comprehensive analysis of PPARÎ±-dependent regulation of hepatic lipid metabolism by expression profiling - 3; GSE8295: Comprehensive analysis of PPARÎ±-dependent regulation of hepatic lipid metabolism by expression profiling - 4; GSE8302: Comprehensive analysis of PPARÎ±-dependent regulation of hepatic lipid metabolism by expression profiling - 5; PPARalpha is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARalpha in hepatic lipid metabolism, many PPARalpha-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARalpha-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARalpha target genes, livers from several animal studies in which PPARalpha was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARalpha-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARalpha-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein beta polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (HSL, Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Regulation of Pnpla2, Lipe, and Mgll, which are involved in triglyceride hydrolysis, was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARalpha agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARalpha. Our study illustrates the power of transcriptional profiling to uncover novel PPARalpha-regulated genes and pathways in liver. Experiment Overall Design: Refer to individual Series

ORGANISM(S): Rattus norvegicus

SUBMITTER: Guido Hooiveld

PROVIDER: E-GEOD-8316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.

Rakhshandehroo Maryam M Sanderson Linda M LM Matilainen Merja M Stienstra Rinke R Carlberg Carsten C de Groot Philip J PJ Müller Michael M Kersten Sander S

PPAR research 20070101

PPARalpha is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARalpha in hepatic lipid metabolism, many PPARalpha-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARalpha-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARalpha target genes, livers from several animal studies in which PPARalpha was activated a ...[more]

PMID: 18288265

Similar Datasets

Project description:PPARÎ± is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARÎ± in hepatic lipid metabolism, many PPARÎ±-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARÎ±-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARÎ± target genes, livers from several animal studies in which PPARÎ± was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARÎ±-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARÎ±-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein Î² polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARÎ± agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARÎ±. Our study illustrates the power of transcriptional profiling to uncover novel PPARÎ±-regulated genes and pathways in liver. Experiment Overall Design: Primary rat and mouse hepatocytes were incubated in the presence (10 uM) or absence of the synthetic PPARÎ± ligand Wy14643 for 24 hours. Primary human hepatocytes were incubated in the presence (50 uM) or absence of Wy14643 for 12 hours. Total RNA was pooled within groups and hybridized onto Rat Genome 230 2.0 Arrays, Mouse Genome 430 2.0 Arrays or Human Genome U133 Plus 2.0 Arrays.

Project description:PPARÎ± is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARÎ± in hepatic lipid metabolism, many PPARÎ±-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARÎ±-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARÎ± target genes, livers from several animal studies in which PPARÎ± was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARÎ±-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARÎ±-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein Î² polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARÎ± agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARÎ±. Our study illustrates the power of transcriptional profiling to uncover novel PPARÎ±-regulated genes and pathways in liver. Experiment Overall Design: 3-5 months old male pure bred wild-type (129S1/SvImJ) and PPARÎ±-null (129S4/SvJae) mice were used. Experiment Overall Design: Wild-type and PPARÎ±-null mice were treated with the synthetic PPARÎ± ligand Wy14643 (0.1% w/w) mixed in the food, or normal food (control) for 5 days (n=4 per group). Liver total RNA from biological replicates was hybridized onto Affymetrix mouse genome 430 2.0 GeneChip arrays. Experiment Overall Design: Five microgram total RNA was labelled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix's protocols.

Project description:PPARÎ± is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARÎ± in hepatic lipid metabolism, many PPARÎ±-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARÎ±-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARÎ± target genes, livers from several animal studies in which PPARÎ± was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARÎ±-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARÎ±-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein Î² polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARÎ± agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARÎ±. Our study illustrates the power of transcriptional profiling to uncover novel PPARÎ±-regulated genes and pathways in liver. Experiment Overall Design: 3-5 months old male pure bred wild-type (129S1/SvImJ) and PPARÎ±-null (129S4/SvJae) mice were used. Experiment Overall Design: Fed mice were killed at the end of the dark cycle (wild-type and PPARÎ±-null mice; n=5 per group), mice were fasted for 24h before sacrifice (wild-type and PPARÎ±-null mice; n=5 per group). Liver total RNA of pooled samples (within groups) was hybridized onto Affymetrix MOE430A GeneChip arrays. Experiment Overall Design: Five microgram total RNA was labelled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix's protocols.

Project description:PPARÎ± is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARÎ± in hepatic lipid metabolism, many PPARÎ±-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARÎ±-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARÎ± target genes, livers from several animal studies in which PPARÎ± was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARÎ±-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARÎ±-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein Î² polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARÎ± agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARÎ±. Our study illustrates the power of transcriptional profiling to uncover novel PPARÎ±-regulated genes and pathways in liver. Experiment Overall Design: 3-5 months old male pure bred wild-type (129S1/SvImJ) and PPARÎ±-null (129S4/SvJae) mice were used. Experiment Overall Design: Wild-type and PPARÎ±-null mice were treated with the synthetic PPARÎ± ligand WY14643 (0.1% w/w) mixed in the food, or normal food (control) for 5 days (n=5 per group). Liver total RNA of pooled samples (within groups) was hybridized onto Affymetrix MOE430A GeneChip arrays. Experiment Overall Design: Five microgram total RNA was labelled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix's protocols.

Project description:PPARÎ± is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARÎ± in hepatic lipid metabolism, many PPARÎ±-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARÎ±-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARÎ± target genes, livers from several animal studies in which PPARÎ± was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARÎ±-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARÎ±-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein Î² polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARÎ± agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARÎ±. Our study illustrates the power of transcriptional profiling to uncover novel PPARÎ±-regulated genes and pathways in liver. Experiment Overall Design: 3-5 months old male pure bred wild-type (129S1/SvImJ) and PPARÎ±-null (129S4/SvJae) mice were used. Experiment Overall Design: Wild-type and PPARÎ±-null mice fasted for 4 hours received a single dose of WY14643 (400 Î¼l of 10 mg/ml WY14643) or vehicle and were killed 6 hours later (n=3-5 per group). Liver total RNA from biological replicates was hybridized onto Affymetrix mouse genome 430 2.0 GeneChip arrays. Experiment Overall Design: Five microgram total RNA was labelled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix's protocols.

Dataset Information

Transcription profiling of liver from PPARalpha knockout mice: PPARa -dependent regulation of hepatic lipid metabolism by expression profiling (GEO Super series)

Publications

Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.

Similar Datasets

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