Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on gene expression in adipose tissue of type 2 diabetic patients. Diabetic patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. Adipose tissue biopsies were taken before and after the treatment.
Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on insulin sensitivity in the adipose tissue of type 2 diabetic patients. Diabetic patients were submitted to a 3 hours hyperinsulinemic- euglycemic clamp. Adipose tissue biopsies were taken before and after the clamp, labelled A & B respectively. Then, the patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. After the treatment, all the patients were submitted to a second 3 hours hyperinsulinemic-euglycemic clamp. Adipose tissue biopsies were taken before and after the clamp, labelled C & D respectively.
Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on insulin sensitivity in the muscle of type 2 diabetic patients. Ten diabetic patients were submitted to a 3 hours euglycemic-hyperinsulinemic clamp. Skeletal muscle biopsies were taken before and after the clamp. Samples from the same patients (obtained before and after the clamp) were hybridized on the same microarray. Biopsie taken before the clamp was considered as the control. Then, the patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. After the treatment, all the patients were submitted to a second 3 hours euglycemic-hyperinsulinemic clamp. Skeletal muscle biopsies for 7 patients were taken before and after the clamp. Samples from the same patients (obtained before and after the clamp) were hybridized on the same microarray. Biopsie taken before the clamp was considered as the control. Set of arrays that are part of repeated experiments Compound Based Treatment: patient biopsies taken before (no) and after (yes) rosiglitazone (TZD) treatment`
Project description:The purpose of this experiment was to determine the murine white adipose expression traits that were changed in response to treatment with Rosiglitazone. Keywords: drug treatment response signature
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.
Project description:White adipose tissue regulates metabolism; the importance of this control is highlighted by the ongoing pandemic of obesity and associated complications such as diabetes, atherosclerosis, and cancer. White adipose tissue maintenance is a dynamic process, very little is known about how pharmacologic stimuli affect such plasticity. Combining in vivo lineage marking and BrdU labeling strategies, we found that rosiglitazone, a member of the thiazolidinedione class of glucose-lowering medicines, markedly increases the evolution of adipose progenitors into adipocytes. Notably, chronic rosiglitazone administration disrupts the adipogenic and self-renewal capacities of the stem cell compartment and alters its molecular characteristics. These data unravel unknown aspects of adipose dynamics and provide a basis to manipulate the adipose lineage for therapeutic ends. The goal of this gene expression array was to identify changes in molecular expression in adipose progenitors isolated from mice that underwent two-month rosiglitazone treatment. Adipose SV GFP+ cells (adipose progenitors) were FACS-isolated from adult AdipoTrak mice that had been treated with or without rosiglitazone (0.0075%) for 2 months. RNAs isolated from these cells were used for microarray. Each cohort contains 3-4 mice, each experimental group (-TZD and +TZD) contains 3 cohorts.
Project description:White adipose tissue regulates metabolism; the importance of this control is highlighted by the ongoing pandemic of obesity and associated complications such as diabetes, atherosclerosis, and cancer. White adipose tissue maintenance is a dynamic process, very little is known about how pharmacologic stimuli affect such plasticity. Combining in vivo lineage marking and BrdU labeling strategies, we found that rosiglitazone, a member of the thiazolidinedione class of glucose-lowering medicines, markedly increases the evolution of adipose progenitors into adipocytes. Notably, chronic rosiglitazone administration disrupts the adipogenic and self-renewal capacities of the stem cell compartment and alters its molecular characteristics. These data unravel unknown aspects of adipose dynamics and provide a basis to manipulate the adipose lineage for therapeutic ends. The goal of this gene expression array was to identify changes in molecular expression in adipose progenitors isolated from mice that underwent two-month rosiglitazone treatment.
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice.
Project description:Diabetic nephropathy (DN) is characterized by metabolic disorder and inflammation. However, the regulatory effects that long noncoding RNAs (lncRNAs) have on the pathogenesis of DN and on the efficacy of rosiglitazone treatment has yet to be clearly defined. Herein, we performed unbiased RNA sequencing to characterize the transcriptomic profiles in db/db diabetic mouse model with or without rosiglitazone treatment that served to improve the phenotypes of DN. Differential expression analysis revealed that those genes that had their expression restored following treatment with rosiglitazone are likely involved in protection against DN. Our data elucidate the novel renoprotective molecular mechanism of PPARγ agonists and propose lncRNA targets for diabetic nephropathy treatment.