Pioglitazone, rosiglitazone and troglitazone treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1458 | GEO | 2004/08/01
SECONDARY ACCESSION(S): PRJNA90011
REPOSITORIES: GEO
Similar Datasets
Project description:3T3-L1 cells treated 24 hours with either 0.1% DMSO, 20uM pioglitazone, 1uM rosiglitazone or 20uM troglitazone
2007-10-09 | E-GEOD-1458 | biostudies-arrayexpress
Project description:Pioglitazone, rosiglitazone and troglitazone treatment
| PRJNA90011 | ENA
Project description:The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.
2018-05-05 | GSE68604 | GEO
Project description:The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.
2018-05-05 | GSE68592 | GEO
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days. Adipose tissue (epididymal), skeletal muscle (gastrocnemius), and liver were harvested from lean (LC) and insulin resistant, obese Zucker rats untreated (FC) or treated with one of four PPARγ ligands (pioglitazone [Pio], rosiglitazone [Rosi], troglitazone [Tro], and AG035029 [AG]).
2011-02-11 | E-GEOD-21329 | biostudies-arrayexpress
Project description:Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).
2012-05-04 | GSE37534 | GEO
Project description:Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone, whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone and yield knowledge as to the causative nature of rosiglitazone-associated cardiac hypertrophy.
2014-06-30 | GSE48977 | GEO
Project description:Goal of the experiment: To examine differential gene expression in the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice treated with vehicle or pioglitazone. Brief description of the experiment: The objective of this study was to use whole mouse genome DNA microarrays (Codelink) to examine gene expression the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice. Women with polycystic ovary syndrome (PCOS) treated with thiazolidinediones (TZD), such as pioglitazone, show reduced androgen levels and improved ovulatory function. Recent evidence suggests that TZD, acting via peroxisome proliferator-activated receptor gamma (PPAR gamma), alter the expression of ovarian genes involved in insulin/IGF signaling that may account for some of the observed effects. Since TZD can alter the expression of a large variety of genes, there may be other mechanisms involved in the improvement of ovarian function with TZD treatment. Lethal yellow (LY) mice exhibit progressive obesity, reproductive dysfunction, and altered metabolic regulation (e.g. insulin and leptin resistance) similar to women with PCOS. This study was designed to test the hypothesis that prolonged treatment of aging LY mice with pioglitazone would alter the expression of ovarian genes involved in reproduction. Beginning at 120-days and continuing until 180-days of age, female LY mice received daily oral doses of either 0.1 mg pioglitazone (n = 4) or an equal volume of vehicle (0.1 ml 100% DMSO; n = 4). At the end of the treatment regimen, ovaries were removed and RNA extracted. Total RNA extracts were run individually on Codelink Mouse Whole Genome Bioarrays (GE). Relative gene expression was compared between treatments by t-test using GeneSpring software. Keywords: mouse, drug treatment Experimental factors: drug treatment Keywords: drug treatment
2008-07-08 | GSE8806 | GEO
Project description:Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD). All gene expression profiles were obtained from highly purified (double-sorted) T cell populations sorted by flow cytometry. To reduce variability, cells from multiple mice were pooled. Triplicates were generated for all groups. Raw data were preprocessed with the RMA algorithm in GenePattern and averaged expression values were used for analysis.
2012-05-03 | E-GEOD-37534 | biostudies-arrayexpress
Project description:Here we report, for the first time, the acute effects of the synthetic PPARγ agonist rosiglitazone on the transcriptional network of PPARγ in adipocytes. Treatment with Rosiglitazone for 1 hour leads to acute transcriptional activation as well as repression of a number of genes as determined by genome-wide RNA polymerase II occupancy. Unlike what has been shown for many other nuclear receptors, agonist treatment does not lead to major changes in the occurrence of PPARγ binding sites. However, rosiglitazone promotes PPARγ occupancy at many preexisting sites, and this is paralleled by increased occupancy of the mediator subunit MED1. The increase in PPARγ and MED1 binding is correlated with an increase in transcription of nearby genes indicating that rosiglitazone, in addition to activating the receptor, also promotes its association with DNA, and that this is causally linked to recruitment of mediator and activation of genes. Notably, both Rosiglitazone-activated and -repressed genes are induced during adipogenesis. However, Rosiglitazone-activated genes are markedly more associated with PPARγ than repressed genes and are highly dependent on PPARγ for expression in adipocytes. By contrast, repressed genes are associated with the other key adipocyte transcription factor CCAAT-Enhancer binding protein (C/EBPα), and their expression is more dependent on C/EBPα. This suggests that the relative occupancies of PPARγ and C/EBPα are critical for whether genes will be induced or repressed by PPARγ agonist. Examination of binding of PPARγ, C/EBPα, RNAPII, CBP and MED1 in mature 3T3-L1 adipocytes treated with 1 μM Rosiglitazone and/or 0.1% DMSO for 1 hour.
2013-08-01 | E-GEOD-49423 | biostudies-arrayexpress