Search results for "ROSIGLITAZONE"

showing 10 items of 26 documents

Glycemic Durability of Rosiglitazone, Metformin, or Glyburide Monotherapy

2006

BACKGROUND: The efficacy of thiazolidinediones, as compared with other oral glucose-lowering medications, in maintaining long-term glycemic control in type 2 diabetes is not known. METHODS: We evaluated rosiglitazone, metformin, and glyburide as initial treatment for recently diagnosed type 2 diabetes in a double-blind, randomized, controlled clinical trial involving 4360 patients. The patients were treated for a median of 4.0 years. The primary outcome was the time to monotherapy failure, which was defined as a confirmed level of fasting plasma glucose of more than 180 mg per deciliter (10.0 mmol per liter), for rosiglitazone, as compared with metformin or glyburide. Prespecified secondary…

Malemedicine.medical_specialtyUrologyKaplan-Meier EstimateType 2 diabetesPharmacologyWeight GainRosiglitazoneGlibenclamidechemistry.chemical_compoundDouble-Blind MethodDiabetes mellitusGlyburidemedicineHumansHypoglycemic AgentsProportional Hazards ModelsGlycemicGlycated HemoglobinGlycemic efficacyWaist-Hip Ratiobusiness.industryCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseMetforminMetforminTreatment OutcomeDiabetes Mellitus Type 2chemistryCardiovascular DiseasesFemaleThiazolidinedionesGlycated hemoglobinbusinessRosiglitazonemedicine.drugNew England Journal of Medicine
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No Improvement of High-Density Lipoprotein (HDL) Vasorelaxant Effect Despite Increase in HDL Cholesterol Concentration in Type 2 Diabetic Patients Tr…

2014

Abstract Context: High-density lipoproteins (HDLs) from type 2 diabetic patients are unable to counteract the inhibitory effect of oxidized low-density lipoproteins (ox-LDLs) on vasorelaxation. We hypothesized that glitazones, which improve glycemic control and dyslipidemia, could correct this abnormality. Objectives and Design: We compared the ability of HDL from controls (n = 12) and from type 2 diabetic patients before and after 6 months of treatment with either rosiglitazone (n = 11) or pioglitazone (n = 8) to counteract the inhibitory effect of ox-LDL on vasodilatation of rabbit aorta rings. Results: Rosiglitazone induced a decrease in hemoglobin A1c (7.7% ± 1.1% vs 9.8% ± 1.0%, P = .0…

Malemedicine.medical_specialtymedicine.drug_classEndocrinology Diabetes and MetabolismClinical BiochemistryContext (language use)BiochemistryRosiglitazonechemistry.chemical_compoundEndocrinologyHigh-density lipoproteinInternal medicineDiabetes mellitusmedicineAnimalsHumansHypoglycemic AgentsThiazolidinedioneAortaAgedDyslipidemiasPioglitazoneCholesterolbusiness.industryCholesterol HDLBiochemistry (medical)Middle Agedmedicine.diseaseLipoproteins LDLVasodilationEndocrinologyDiabetes Mellitus Type 2chemistryFemaleThiazolidinedionesEndothelium VascularRabbitsLipoproteins HDLRosiglitazonebusinessPioglitazoneDyslipidemiamedicine.drugThe Journal of Clinical Endocrinology & Metabolism
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The Blood–Brain Barrier as a Target in Traumatic Brain Injury Treatment

2014

Traumatic brain injury (TBI) is one of the most frequent causes of death in the young population. Several clinical trials have unsuccessfully focused on direct neuroprotective therapies. Recently immunotherapeutic strategies shifted into focus of translational research in acute CNS diseases. Cross-talk between activated microglia and blood–brain barrier (BBB) could initiate opening of the BBB and subsequent recruitment of systemic immune cells and mediators into the brain. Stabilization of the BBB after TBI could be a promising strategy to limit neuronal inflammation, secondary brain damage and acute neurodegeneration. This review provides an overview on the pathophysiology of TBI and brain…

Pathologymedicine.medical_specialtyTraumatic brain injuryPeroxisome Proliferator-Activated ReceptorsBrain EdemaInflammationBrain damageBlood–brain barrierNeuroprotectionRosiglitazoneReceptors GlucocorticoidmedicineHumansHypoglycemic AgentsMyosin-Light-Chain KinaseNeuroinflammationInflammationPioglitazoneMicrogliabusiness.industryNeurodegenerationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseCell HypoxiaNeuroprotective Agentsmedicine.anatomical_structurenervous systemBlood-Brain BarrierBrain InjuriesThiazolidinedionesmedicine.symptombusinessNeuroscienceArchives of Medical Research
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Incidence of Diabetes Following Ramipril or Rosiglitazone Withdrawal

2011

OBJECTIVE To examine the impact of withdrawing rosiglitazone and ramipril medication on diabetes incidence after closeout of the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) trial. RESEARCH DESIGN AND METHODS The 3,366 DREAM subjects at trial end who had not developed diabetes while taking double-blind study medication were transferred to single-blind placebo for 2 to 3 months before undergoing an oral glucose tolerance test. Glycemic status was analyzed for the trial plus washout period and for the washout period alone. RESULTS Following median (interquartile range) 71 (63–86) days drug withdrawal, overall glycemic status remained modestly improved in t…

RamiprilAdultMalemedicine.medical_specialtyEndocrinology Diabetes and Metabolism030209 endocrinology & metabolism030204 cardiovascular system & hematologyPlaceboRosiglitazone03 medical and health sciencesDrug withdrawal0302 clinical medicineRamiprilInterquartile rangeInternal medicineDiabetes mellitusInternal MedicinemedicineHumansHypoglycemic AgentsGlycemicOriginal ResearchAdvanced and Specialized Nursingbusiness.industryIncidence (epidemiology)IncidenceClinical Care/Education/Nutrition/Psychosocial ResearchMiddle Agedmedicine.disease3. Good healthSurgerySubstance Withdrawal SyndromeTreatment OutcomeDiabetes Mellitus Type 2FemaleThiazolidinedionesRosiglitazonebusinessmedicine.drugFollow-Up StudiesDiabetes Care
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An Update on the Current and Emerging Use of Thiazolidinediones for Type 2 Diabetes.

2022

Guidelines have increasingly stressed the concept that adequate glycemic control is required to prevent or decrease the macro- and microvascular complications of type 2 diabetes mellitus (T2DM). PPAR-gamma agonists (“glitazones”) are no longer prioritized due to their effects on heart failure. However, the association between these drugs and innovative therapies could be a valuable tool to attenuate the risk factors of the metabolic syndrome. Glitazones are used for the treatment of diabetes and associated comorbidities. There is substantial scientific evidence demonstrating the effect of glitazones at a cardiometabolic level, as well as on hematological and neurological pathologies that po…

RosiglitazoneDiabetes Mellitus Type 2PioglitazonePeroxisome Proliferator-Activated ReceptorsHumansHypoglycemic AgentsThiazolidinedionescardiovascular risk metabolic syndrome pioglitazone type 2 diabetes mellitusGeneral MedicineMedicina (Kaunas, Lithuania)
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A compound-based proteomic approach discloses 15-ketoatractyligenin methyl ester as a new PPARγ partial agonist with anti-proliferative ability

2017

AbstractProteomics based approaches are emerging as useful tools to identify the targets of bioactive compounds and elucidate their molecular mechanisms of action. Here, we applied a chemical proteomic strategy to identify the peroxisome proliferator-activated receptor γ (PPARγ) as a molecular target of the pro-apoptotic agent 15-ketoatractyligenin methyl ester (compound 1). We demonstrated that compound 1 interacts with PPARγ, forms a covalent bond with the thiol group of C285 and occupies the sub-pocket between helix H3 and the β-sheet of the ligand-binding domain (LBD) of the receptor by Surface Plasmon Resonance (SPR), mass spectrometry-based studies and docking experiments. 1 displayed…

Transcriptional Activation0301 basic medicinenatural productTime FactorsPeroxisome proliferator-activated receptorApoptosisLigandsPartial agonistArticleRosiglitazonePPAR_gammaJurkat Cells03 medical and health sciencesTransactivation0302 clinical medicineproteomicsHumansBinding siteReceptorMode of actionPI3K/AKT/mTOR pathwayCell Proliferationchemistry.chemical_classificationBinding SitesMultidisciplinaryProtein StabilityProtein Proliferator-Activated-Receptor PPARs Ligand-Binding Domain Chemical Proteomics Accurate Docking Pi3k/Akt Pathway Drug Discovery Anticancer compoundsReproducibility of ResultsEstersSurface Plasmon ResonanceMolecular Docking SimulationPPAR gammaKineticsHEK293 Cells030104 developmental biologychemistryBiochemistryDocking (molecular)030220 oncology & carcinogenesisThermodynamicsThiazolidinedionesproteomics PPAR_gamma natural productDiterpenes KauraneHT29 CellsScientific Reports
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A role for peroxisome proliferator-activated receptor gamma in resveratrol-induced colon cancer cell apoptosis.

2014

Scope Resveratrol may function as a chemopreventive agent. A recent clinical study demonstrates a reduction in tumor cell proliferation in colorectal patients receiving repeated oral ingestion of resveratrol. However, gaps remain in our knowledge of the molecular mechanisms by which resveratrol exerts its chemopreventive effect. We have previously demonstrated that resveratrol induces apoptosis in colon cancer cells and that resveratrol can sensitize chemoresistant colon cancer cells to various drugs. Based on its ability to activate peroxisome proliferator-activated receptor gamma (PPARγ) in colon cancer cells, we sought to determine the implication of this nuclear transcription factor in …

endocrine system diseasesColorectal cancerPeroxisome proliferator-activated receptorApoptosisPharmacologyResveratrolresveratrolMESH: ThiazolidinedionesPPAR[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound0302 clinical medicineMESH: StilbenesStilbenesMESH : Cell Proliferation[ SHS.INFO ] Humanities and Social Sciences/Library and information sciencesAnilidesskin and connective tissue diseaseschemistry.chemical_classification0303 health sciencesfood and beveragesCell cycle3. Good healthMESH : ThiazolidinedionesMESH : Colonic Neoplasmscolon cancer030220 oncology & carcinogenesisColonic NeoplasmsS Phase Cell Cycle CheckpointsRosiglitazonehormones hormone substitutes and hormone antagonistsBiotechnologymedicine.drugMESH : PPAR gammaMESH: Cell Line Tumor[SHS.INFO]Humanities and Social Sciences/Library and information sciences[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Anilides[SHS.INFO] Humanities and Social Sciences/Library and information sciencesMESH : AnilidesMESH : StilbenesRosiglitazone03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerCell Line TumorMESH: Cell Proliferationmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH : S Phase Cell Cycle Checkpoints[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologypolyphenols030304 developmental biologyCell ProliferationMESH: Colonic NeoplasmsMESH: HumansCell growthMESH : Cell Line Tumor[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyorganic chemicalsMESH: ApoptosisMESH : Humansmedicine.diseasePPAR gammaMESH: S Phase Cell Cycle CheckpointschemistryMESH: PPAR gammaApoptosisCancer cellThiazolidinedionesMESH : ApoptosisFood Science
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The differential effects of thiazolidindiones on atherogenic dyslipidemia in type 2 diabetes: what is the clinical significance?

2008

Diabetic dyslipidemia is typically characterized by an increase in plasma triglycerides, a decrease in high-density lipoprotein cholesterol and a concomitant increase in atherogenic small dense low-density lipoproteins. Thiazolidindiones are able to lower the levels of fasting glucose and glycated hemoglobin significantly by improving insulin sensitivity, as well as improving some aspects of diabetic dyslipidemia: total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol tend to increase while triglycerides are generally decreased.This paper reviewed the effects of pioglitazone and rosiglitazone on atherogenic diabetic dyslipidemia, in particular on sma…

medicine.medical_specialty10265 Clinic for Endocrinology and Diabetology610 Medicine & healthType 2 diabetesRosiglitazonechemistry.chemical_compoundDiabetes mellitusInternal medicinemedicine2736 Pharmacology (medical)HumansHypoglycemic AgentsPharmacology (medical)Clinical significancecardiovascular risk dense low-density lipoprotein diabetes low-density lipoprotein size pioglitazone rosiglitazone smallTriglyceridesDyslipidemiasPharmacologyAtherogenic dyslipidemiaPioglitazonebusiness.industryThiazolidindionesAtherogenic dyslipidemiaGeneral Medicinemedicine.diseaseLipoproteins LDLEndocrinology3004 PharmacologychemistryDiabetes Mellitus Type 2lipids (amino acids peptides and proteins)ThiazolidinedionesGlycated hemoglobinbusinessRosiglitazoneLipoproteins HDLPioglitazoneBiomarkersmedicine.drugLipoprotein
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Different effects of pioglitazone and rosiglitazone on lipid metabolism in mouse cultured liver explants.

2010

Background Pioglitazone (PIO) and rosiglitazone (ROSI) are widely used as oral antidiabetic agents for treatment of type 2 diabetes. Although these medications exert similar effects on blood glucose, recent clinical studies indicated that PIO has a more pronounced beneficial effect on lipid parameters than ROSI. In order to get further insight into the lipid effects of both drugs, we tested whether PIO, compared to ROSI, could exert direct effects on lipid liver metabolism in relation with plasma lipids. Methods We performed in vitro studies using mice liver slices incubated 21 h either with ROSI (1 µmol/L) or PIO (7.5 µmol/L). Results We showed that both glitazones slightly reduced HMG-CoA…

medicine.medical_specialtyApolipoprotein BEndocrinology Diabetes and MetabolismRosiglitazoneTissue Culture Techniqueschemistry.chemical_compoundMiceEndocrinologyInternal medicineInternal MedicinemedicineAnimalsHumansScavenger receptorGlycated HemoglobinbiologyPioglitazoneCholesterolbusiness.industryCholesterol HDLLipid metabolismLipaseLipid MetabolismMice Inbred C57BLPPAR gammaEndocrinologychemistryLiverLipogenesisbiology.proteinThiazolidinedionesHepatic lipaseRosiglitazonebusinessPioglitazonemedicine.drugDiabetes/metabolism research and reviews
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PPAR in Cardiovascular Disorders

2016

Peroxisome proliferation-activated receptors (PPARs) are ligand-inducible transcription factors that, upon binding their ligands, translocate into the nucleus, where they regulate transcription of numerous genes that have the peroxisome proliferator response element (PPRE) in the promoter region [1]. In humans, there are 3 PPAR isoforms: PPAR-α, PPAR-β/δ, and PPAR-γ. The isoforms have partially overlapping spectra of activity and are differently expressed in organs and tissues [2]. PPAR-α is expressed mostly in tissues characterized by high catabolic activity, including skeletal muscle, liver, proximal tubular cells in kidneys, and brown fat. This PPAR isoform regulates components of β-oxid…

medicine.medical_specialtyArticle SubjectPeroxisome proliferator-activated receptor030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationInternal medicineDrug DiscoverymedicineGlucose homeostasisPharmacology (medical)Beta oxidationlcsh:QH301-705.5chemistry.chemical_classificationFatty acid metabolismLipid metabolismPeroxisomeEndocrinologyEditorialchemistrylcsh:Biology (General)Rosiglitazonemedicine.drugPPAR Research
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