Expression data from the adipose tissue of mice fed a normal diet and a high fat diet.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE36492 | GEO | 2013/01/30
SECONDARY ACCESSION(S): PRJNA153533
REPOSITORIES: GEO
Similar Datasets
Project description:To identify novel Peroxisome Proliferator-Activated Receptor gamma (PPARg) responsive secretory and/or transmembrane genes that is related to obesity, we integrated the expression data from the adipose tissue derived from obese mice with the other two data sets: expression profiling of adipocyte differentiation using ST2 cells and siRNA-mediated knockdown of Pparg during ST2 cell adipogenesis. We used microarrays to detect the up-regulated genes in adipose tissue derived from mice fed a high fat diet compared to a control. Total RNA from adipose tissue was obtained and from mice fed a high fat diet HFD32 (MOUSE_HFD) from 6 week-old to 18 week-old, or a normal diet CE-2 (MOUSE_ND) as a control. Pooled RNAs of each three animals were analyzed by the Affymetrix GeneChip microarray system.
2013-01-30 | E-GEOD-36492 | biostudies-arrayexpress
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes.
2013-12-31 | GSE20371 | GEO
Project description:Actin dynamics, mediated by various actin-binding proteins, plays an important role in adipocyte differentiation. We investigated the role of coactosin-like F-actin binding protein (Cotl1) in adipocyte differentiation in vitro and in vivo. Cotl1 expression level was increased during adipocyte differentiation in mouse 3T3-L1 cells and primary cultured adipose-derived stem cells (ADSCs) and during weight gain in adipose tissues. However, Cotl1 deficient in 3T3-L1 and ADSCs inhibited adipocyte differentiation, and Cotl1-/- mice displayed resistance to high-fat diet (HFD)-induced weight gain, hepatic steatosis and adipocyte enlargement compared to HFD-fed wild type (WT) mice. Ingenuity Pathway Analysis of RNA-sequencing in adipose tissues of HFD-WT and HFD-Cotl1-/- mice predicted complicated relationships between Cotl1, differentiation of adipocytes, obesity and organization of actin cytoskeleton. Particularly, peroxisome proliferator-activated receptor gamma (Pparg) emerged as a central player, with Cotl1 influencing Pparg expression, consequently regulating adipocyte differentiation. These findings suggest Cotl1 as a pivotal regulator of terminal adipocyte differentiation by modulating adipogenic genes.
2025-04-08 | GSE293445 | GEO
Project description:Peroxisome proliferator-activated receptor g (PPARg) is a nuclear receptor that is a vital regulator of adipogenesis, insulin sensitivity, and lipid metabolism. Activation of PPARg by antidiabetic thiazolidinediones (TZD) reverses insulin resistance but also leads to weight gain that limits the use of these drugs. There are two main PPARg isoforms, but the specific functions of each are not established. Here we generated mouse lines in which endogenous PPARg1 and PPARg2 were epitope-tagged to interrogate isoform-specific genomic binding, and mice deficient in either PPARg1 or PPARg2 to assess isoform-specific gene regulation. Strikingly, although PPARg1 and PPARg2 contain identical DNA binding domains, we uncovered isoform-specific genomic binding sites in addition to shared sites. Moreover, PPARg1 and PPARg2 regulated different set of genes in adipose tissue depots, suggesting distinct roles in adipocyte biology. Indeed, mice with selective deficiency of PPARg1 maintained body temperature better than wild type or PPARg2-deficient mice. Most remarkably, although TZD treatment improved glucose toleranceinsulin resistance in mice lacking either PPARg1 or PPARg2, the PPARg1-deficient mice were protected from TZD-induced body weight gain compared to PPARg2-deficient mice. Thus, PPARg isoforms have specific and separable metabolic functions that may be targeted to improve therapy for insulin resistance and diabetes.
2022-03-25 | GSE186277 | GEO
Project description:PPARg and C/EBPa cooperate to control preadipocyte differentiation (adipogenesis). However, the factors that regulate PPARg and C/EBPa expression during adipogenesis remain largely unclear. Here we show PTIP, a protein that associates with histone H3K4 methyltransferases, regulates PPARg and C/EBPa expression in mouse embryonic fibroblasts (MEFs) and during preadipocyte differentiation. PTIP deletion in MEFs leads to marked decreases of PPARg expression and PPARg-stimulated C/EBPα expression. Further, PTIP is essential for induction of PPARg and C/EBPa expression during preadipocyte differentiation. Deletion of PTIP impairs the enrichment of H3K4 trimethylation and RNA polymerase II on PPARg and C/EBPa promoters. Accordingly, PTIP-/- MEFs and preadipocytes all show striking defects in adipogenesis. Furthermore, rescue of the adipogenesis defect in PTIP-/- MEFs requires co-expression of PPARg and C/EBPa. Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight in mice. Thus, by regulating PPARg and C/EBPa expression, PTIP plays a critical role in adipogenesis.
2009-05-29 | GSE16263 | GEO
Project description:Oryctolagus cuniculus PPARG, Oryctolagus cuniculus peroxisome proliferator activated receptor gamma (PPARG), mRNA. [Source:RefSeq mRNA;Acc:NM_001082148], is expressed in 1 baseline experiment(s);
| ENSOCUG00000013194 | ExpressionAtlas
Project description:PPARg and C/EBPa cooperate to control preadipocyte differentiation (adipogenesis). However, the factors that regulate PPARg and C/EBPa expression during adipogenesis remain largely unclear. Here we show PTIP, a protein that associates with histone H3K4 methyltransferases, regulates PPARg and C/EBPa expression in mouse embryonic fibroblasts (MEFs) and during preadipocyte differentiation. PTIP deletion in MEFs leads to marked decreases of PPARg expression and PPARg-stimulated C/EBPα expression. Further, PTIP is essential for induction of PPARg and C/EBPa expression during preadipocyte differentiation. Deletion of PTIP impairs the enrichment of H3K4 trimethylation and RNA polymerase II on PPARg and C/EBPa promoters. Accordingly, PTIP-/- MEFs and preadipocytes all show striking defects in adipogenesis. Furthermore, rescue of the adipogenesis defect in PTIP-/- MEFs requires co-expression of PPARg and C/EBPa. Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight in mice. Thus, by regulating PPARg and C/EBPa expression, PTIP plays a critical role in adipogenesis. To identify PTIP-regulated genes, immortalized PTIP conditional knockout PTIPflox/flox MEFs were infected with retroviruses expressing either Cre recombinase or vector alone. We prepared duplicated RNAs from either vector or Cre infected cells (PTIP+/+ or PTIP-/-) for 4 affymetrix microarrays.
2009-05-29 | E-GEOD-16263 | biostudies-arrayexpress
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes. Wild type mouse embryonic fibroblasts (MEFs) stably infected with retroviruses MSCVpuro expressing PPARd were plated at 0.5 million per 10 cm dish. After overnight incubation, cells were treated with 100nM GW501516 for 0h, 2h, 8h and 48h. Cells were collected at subconfluent condition. Total RNAs were sequentially purified with Trizol (Invitrogen) and RNeasy kit (Qiagen) and analyzed in triplicate on Mouse Genome 430 2.0 Array (Affymetrix) at NIDDK Microarray Core Facility following standard protocols.
2013-12-31 | E-GEOD-20371 | biostudies-arrayexpress
Project description:Oral squamous cell carcinoma (OSCC), one of the most common malignant tumor in head and neck, which is regulated by cellular factors. Among them, peroxisome proliferator activated receptor gamma (PPARG) has been reported to have main functions in the regulation of several human cancer cells, including OSCC. However, its regulatory mechanism remains unclear. Here, we performed a functional genomics study of PPARG overexpressing OSCC by using RNA-seq.
2023-09-01 | GSE186635 | GEO
Project description:"Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile"
Monica Viladomiu1,2, Raquel Hontecillas1,2, Mireia Pedragosa1,2, Adria Carbo1,2, Stefan Hoops1,2, Pawel Michalak4,5, Katarzyna Michalak4, Richard L. Guerrant2,3, James K. Roche2,3, Cirle A. Warren2,3, Josep Bassaganya-Riera1,2*
1) Nutritional Immunology and Molecular Medicine Laboratory, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 2) Center for Modeling Immunity to Enteric Pathogens, Virginia Tech, Blacksburg, Virginia, United States of America, 3) Division of Infectious Disease and International Health, Center for Global Health, University of Virginia, Charlottesville, Virginia, United States of America, 4) Medical Informatics and Systems Division, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 5) Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, United States of America
E-mail: jbassaga@vt.edu
This model represents the interaction between Cdiff, miRNA146b, NCOA4, PPARg, IL10 and IL17. Simulation studies show an aberrant expression of miRNA146b with increasing concentrations of Cdiff over time, which results in decreased PPARg activation due to NCOA4 inhibition. As a final result, PPARg is unable to modulate effector and regulatory responses, since results show an upregulation of IL17 expression and downregulation of IL10 production.
2005-01-01 | MODEL1210260004 | BioModels