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Reseveratrol and Rosiglitazone regulation of blood gene expression in ZDF rats

ABSTRACT: The goal of this work was to examine if reserveratrol or rosiglitazone treatment could improve the metabolic status of obese male ZDF rats after 6 weeks. Gene expression was analyzed in several key metabolic tissues, including liver, various white adipose tissue depots, red tibalus muscle, and whole blood.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE93402 | GEO | 2017/02/07

SECONDARY ACCESSION(S): PRJNA360913

REPOSITORIES: GEO

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Reseveratrol and Rosiglitazone regulation of liver gene expression in ZDF rats

Project description:The goal of this work was to examine if reserveratrol or rosiglitazone treatment could improve the metabolic status of obese male ZDF rats after 6 weeks. Gene expression was analyzed in several key metabolic tissues, including liver, various white adipose tissue depots, red tibalus muscle, and peripheral blood mononuclear cells.

2017-02-07 | GSE93403 | GEO

Reseveratrol and Rosiglitazone regulation of red tibialis anterior (red TA) gene expression in ZDF rats

2017-02-07 | GSE93406 | GEO

sRNA sequencing of liver from lean rats and ZDF rats treated with vehicle or colesevelam

Project description:Colesevelam is a bile acid sequestrant approved to treat both hyperlipidemia and type 2 diabetes, but the mechanism for its glucose lowering effects is not fully understood. The aim of this study was to investigate the role of hepatic microRNA’s as regulators of metabolic disease and to investigate the link between the cholesterol and glucose lowering effects of colesevelam. To quantify the impact of colesevelam treatment in rodent models of diabetes, metabolic studies were performed in Zucker Diabetic Fatty (ZDF) rats and db/db mice. Colesevelam treatments significantly decreased plasma glucose levels and increased glycolysis in the absence of changes to insulin levels in ZDF rats and db/db mice. High-throughput sequencing and real-time PCR were used to quantify hepatic miRNA and mRNA changes, and the cholesterol-sensitive miR-96/182/183 cluster was found to be significantly increased in livers from ZDF rats treated with colesevelam compared to vehicle controls. In summary, these results support that colesevelam likely improves glycemic control through hepatic miR-96/182/183, a mechanism that directly links cholesterol and glucose metabolism.

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Muscle Involvement in Preservation of Metabolic Flexibility by Treatment using n-3 PUFA, Rosiglitazone, and a combination of both

Project description:This SuperSeries is composed of the following subset Series: GSE36716: Muscle Involvement in Preservation of Metabolic Flexibility by Treatment using n-3 PUFA or Rosiglitazone in Dietary-Obese Mice GSE36717: Muscle Involvement in Preservation of Metabolic Flexibility by a Combination Treatment using n-3 PUFA and Rosiglitazone in Dietary-Obese Mice Refer to individual Series

2012-09-07 | E-GEOD-36718 | biostudies-arrayexpress

Hepatic transcriptomic analyses revealing the molecular pathogenesis of T2DM associated NAFLD in the ZDF rats

Project description:The ZDF rat, with spontaneous homozygous mutation of the leptin receptor gene (fa/fa), is one of the widely used animal model for studying the human type 2 diabetes mellitus (T2DM). Male ZDF rats have the symptoms of obesity and insulin resistance at a young age, accompanying with impaired islet function. However, their hepatic pathogenesis is still unclear. Based on the successive observations and the transcriptomic analyses of the liver tissue at 22 weeks old, we detected the typical clinical indications of T2DM, severe hepatic metabolic remodeling and the inflammatory liver injury in the ZDF rats. The integrin linked kinase signaling, as well as the endoplasmic reticulum stress and its downstream p38 MAPK signaling, seemed to play crucial roles in it. We have proved the ZDF rats could better simulate the pathogenesis of the human T2DM associated nonalcoholic fatty liver disease (NAFLD), and provided targets and reference for future T2DM studies.

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Cardiac Effects of Rosiglitazone in Male Wistar Rats

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GW7647 and Rosiglitazone treated human differentiated adipocytes

Project description:Objective : This work aimed at characterizing PPARα involvement in metabolism regulation and at comparing PPARα and PPARγ roles in human white adipocytes. Research Design and Methods : Profiling of gene expression alterations was assessed with microarrays and RT-qPCR. Primary cultures of human adipocytes were treated with PPARα agonist GW7647 or PPARγ agonist Rosiglitazone. Western blot were used to determine protein level modifications. Metabolic changes were evaluated with palmitate and glucose oxidation studies and with metabolite measurements. Results : GW7647 induces an upregulation of β-oxidation gene expression and increases palmitate oxidation. Unexpectedly glycolysis was strongly reduced at transcriptional and functional levels by GW7647 while the overall glucose oxidation remains unaltered, leading to a decrease in pyruvate and lactate production. Moreover lipogenesis was downregulated by GW7647 inhibiting triglyceride esterification and de novo lipogenesis. GW7647 induced alterations were abolished by a PPARα antagonist treatment and were clearly different from Rosiglitazone effects. Rosiglitazone had no major impact on glycolysis and β-oxidation but increased glucose incorporation into glycerol backbone of triglycerides. Conclusions : Altogether these results show that PPARα can upregulate β-oxidation in human white adipocytes. Its pharmacological activation may be used to oxidize fatty acids in situ when lipolysis is activated thus preventing their release into systemic circulation. We treated four adipocyte cultures, each one coming from different subjects, with GW7647, Rosiglitazone (ROSI) or DMSO. DMSO treated cells are control samples. Thus we have four paired sample groups for each treatment (GW7647 and ROSI).

2010-04-11 | E-GEOD-15862 | biostudies-arrayexpress

GW7647 and Rosiglitazone treated human differentiated adipocytes

2010-04-11 | GSE15862 | GEO

Effects of rosiglitazone treatment on lipid composition

Project description:Reprograming of 'white' to 'brite' adipocytes with higher oxidative capacity and improved endocrine function represents a potentially important approach to address the dysfunctional adipocyte phenotypes in obesity. We find that chronic treatment with the PPAR? agonist (rosiglitazone, 1 uM for 7days in vitro) in white human adipose tissue induced metabolic changes. Our trancriptome analysis showed that higher mitochondrial and peroxisomal fatty acid oxidation pathways and other genes involved in lipid metabolism including (re)esterification are induced by rosiglitazone treatment. To understand the biochemical basis of brite vs. white human adipocytes, we will perform comprehensive metabolomic profiling of control and rosiglitazone treated tissues using unbiased lipidomics approach.

2017-06-05 | ST000675 | MetabolomicsWorkbench

Rosiglitazone Signature in Mouse White Adipose Tissue

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

2007-02-17 | GSE7027 | GEO

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