Search results for "Hypolipidemic Agents"

showing 10 items of 83 documents

Expression of liver peroxisomal proteins as compared to other organelle marker enzymes in rats treated with hypolipidemic agents.

1990

Abstract Peroxisome proliferation induced by 2 hypolipidemic agents (clofibrate and ciprofibrate) was studied in rats by complementary approaches, ie cell fractionation, electron microscopy, marker enzyme activities, immunoblotting and nucleic acid hybridization techniques. Administration of clofibrates for 2 and 52 weeks in doses of 500 ppm and 50 ppm respectively, or ciprofibrate for 2,28 and 52 weeks in doses of 250, 25 and 25 ppm respectively, did not alter the behavior of the peroxisomes after induction as shown by ultracentrifugation profiles. The peroxisome mass was increased as shown by the purification procedure. Specific enzymes (catalase and mostly cyanide insensitive palmitoyl C…

MaleImmunoblottingMolecular Sequence DataPeroxisome ProliferationMitochondrionCell FractionationMicrobodiesClofibric AcidOrganellemedicineAnimalsClofibrateRNA MessengerHypolipidemic AgentsOrganellesClofibratebiologyBase SequenceEndoplasmic reticulumFibric AcidsRats Inbred StrainsCell BiologyGeneral MedicinePeroxisomeMolecular biologyRats Inbred F344RatsBiochemistryLiverCatalasebiology.proteinCiprofibrateDNA Probesmedicine.drugBiology of the cell
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Effect of hypolipidemic treatment on emerging risk factors in mixed dyslipidemia: a randomized pilot trial

2012

Background The effects of different hypolipidemic treatment strategies on emerging atherosclerosis risk factors remain unknown. Materials and methods This is a prespecified analysis of a prospective, randomized, open-label, blinded end point (PROBE) study (ClinicalTrials.gov identifier: NCT01010516). Patients (n = 100) with mixed dyslipidaemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) or to add-on-statin micronized fenofibrate for a total of 3 months. Results Following 3 months of treatment, low-density lipoprotein (LDL) …

MaleIndolesTime FactorsClinical BiochemistryPilot ProjectsPharmacologyBiochemistryGastroenterologychemistry.chemical_compoundFenofibrateRisk FactorsProspective StudiesRosuvastatin CalciumHypolipidemic AgentsSulfonamidesFenofibratebiologyGeneral MedicineMiddle AgedRosuvastatin CalciumC-Reactive ProteinCardiovascular DiseasesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Laropiprantmedicine.drugAdultmedicine.medical_specialtyStatinmedicine.drug_classNiacinInternal medicinemedicineHumansRosuvastatinAgedApolipoproteins BDyslipidemiasbusiness.industryCholesterolC-reactive proteinnutritional and metabolic diseasesCholesterol LDLAtherosclerosismedicine.diseaseFluorobenzenesPyrimidineschemistry1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessDyslipidemiaEuropean Journal of Clinical Investigation
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Enhanced lipid peroxidation and platelet activation as potential contributors to increased cardiovascular risk in the low-HDL phenotype

2013

Background Low high‐density lipoprotein ( HDL ) levels are major predictors of cardiovascular ( CV ) events, even in patients on statin treatment with low‐density lipoprotein ( LDL ) at target. In animal models HDL s protect LDL from oxidation and blunt platelet activation. Our study aimed to examine whether HDL levels are related to in vivo oxidative stress and platelet activation, as determinants of atherothrombosis. Methods and Results Urinary 8‐iso‐PGF 2α and 11‐dehydro‐TXB 2 , in vivo markers of oxidative stress and platelet activation, respectively, were measured in 65 coronary heart disease (CHD) normocholesterolemic patients with HDL ≤35 mg/ dL , and in 47 CHD patients with HDL &gt…

MaleSettore MED/09 - Medicina InternaCoronary DiseaseDinoprostmedicine.disease_causeLipid peroxidationchemistry.chemical_compoundFenofibrateHDL cholesterolRisk FactorsCoronary Heart Diseaseoxidative stressMyocardial infarctionOriginal ResearchHypolipidemic AgentsplateletHypoalphalipoproteinemiasFenofibrateMiddle AgedAged; Arachidonic Acids; Case-Control Studies; Cholesterol HDL; Coronary Disease; Cross-Sectional Studies; Dinoprost; Exercise; Exercise Therapy; Female; Fenofibrate; Humans; Hypoalphalipoproteinemias; Hypolipidemic Agents; Lipid Peroxidation; Male; Middle Aged; Oxidative Stress; Phenotype; Platelet Activation; Risk Factors; Sedentary Lifestyle; Thromboxane B2; Cardiology and Cardiovascular MedicineExercise TherapyCholesterolPhenotypeSedentary LifestyleFemalelipids (amino acids peptides and proteins)exercise HDL cholesterol oxidative stress plateletCardiology and Cardiovascular Medicinemedicine.drugmedicine.medical_specialtyHDLArachidonic AcidsDiabetes mellitusInternal medicinemedicineHumansPlatelet activationExerciseAgedCreatininebusiness.industryCholesterol HDLCase-control studyPlatelet Activationmedicine.diseaseThromboxane B2Cross-Sectional StudiesEndocrinologychemistryCase-Control StudiesLipid PeroxidationSedentary BehaviorbusinessOxidative stressLipoproteinEuropean Heart Journal
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Remarkable quantitative and qualitative differences in HDL after niacin or fenofibrate therapy in type 2 diabetic patients

2014

Abstract HDL-increasing drugs such as fenofibrate and niacin have failed to decrease the cardiovascular risk in patients with type 2 diabetes. Drug-mediated quantitative and qualitative HDL modifications could be involved in these negative results. To evaluate the quantitative and qualitative effects of niacin and fenofibrate on HDL in patients with type 2 diabetes, a prospective, randomised controlled intervention trial was conducted. Thirty type 2 diabetic patients with low HDL were randomised to receive either fenofibrate (FFB) or niacin + laropiprant (ERN/LPR) as an add-on to simvastatin treatment for 12 weeks according to a crossover design. At the basal point and after each interventi…

MaleSimvastatinIndolesTime FactorsType 2 diabetesHigh-Density Lipoproteins Pre-betaAntioxidantsBasal (phylogenetics)chemistry.chemical_compoundFenofibrateProspective StudiesHypolipidemic AgentsFenofibrateMiddle AgedOxidantsPON1Up-RegulationTreatment OutcomeDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineNiacinmedicine.drugAdultmedicine.medical_specialtyNiacinbehavioral disciplines and activitiesInternal medicinemedicineHumansMetabolomicsParticle SizeAgedDyslipidemiasbusiness.industryCholesterolCholesterol HDLnutritional and metabolic diseasesmedicine.diseaseCrossover studyCross-Sectional StudiesEndocrinologyDiabetes Mellitus Type 2chemistrySpainSimvastatinHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessBiomarkersAtherosclerosis
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Effects of lipid-lowering drugs on high-density lipoprotein subclasses in healthy men-a randomized trial.

2013

Context and Objective Investigating the effects of lipid-lowering drugs on HDL subclasses has shown ambiguous results. This study assessed the effects of ezetimibe, simvastatin, and their combination on HDL subclass distribution. Design and Participants A single-center randomized parallel 3-group open-label study was performed in 72 healthy men free of cardiovascular disease with a baseline LDL-cholesterol of 111±30 mg/dl (2.9±0.8 mmol/l) and a baseline HDL-cholesterol of 64±15 mg/dl (1.7±0.4 mmol/l). They were treated with ezetimibe (10 mg/day, n = 24), simvastatin (40 mg/day, n = 24) or their combination (n = 24) for 14 days. Blood was drawn before and after the treatment period. HDL subc…

MaleSimvastatinlcsh:MedicinePharmacologyBiochemistryLipoprotein MetabolismVascular MedicineSubclasslaw.inventionchemistry.chemical_compoundHigh-density lipoproteinRandomized controlled triallawMedicine and Health SciencesMedicinelcsh:ScienceHypolipidemic AgentsMultidisciplinaryHealthy VolunteersResearch DesignDrug Therapy Combinationlipids (amino acids peptides and proteins)Lipoproteins HDLResearch Articlemedicine.drugAdultmedicine.medical_specialtylipid-lowering drugs high-density lipoprotein healthy menDrug Research and DevelopmentClinical Research DesignLipoproteinsHypercholesterolemiaCardiologyAdipokineContext (language use)Research and Analysis MethodsCardiovascular PharmacologyAdipokinesEzetimibeInternal medicineHumansClinical TrialsPharmacologybusiness.industryCholesterollcsh:RBiology and Life SciencesProteinsnutritional and metabolic diseasesEzetimibeAtherosclerosisGlucoseEndocrinologychemistrySimvastatinAzetidineslcsh:QClinical MedicinebusinessBiomarkersPLoS ONE
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Differential proto-oncogene mRNA induction from rats treated with peroxisome proliferators

1990

After experimental treatment of rats with clofibrate or ciprofibrate, two peroxisomes proliferators with hypolipidemic activity, RNAs were prepared from liver, kidney, heart and brain; hybridization was done with DNA probes for c-myc and c-Ha-ras oncogenes and for cyanide insensitive Acyl CoA oxidase, a peroxisomal protein. c-myc mRNA is highly abundant in liver and at a lower extent in kidney, especially after treatment with ciprofibrate; clofibrate also allows a c-myc mRNA increase, but at a lower extent. c-Ha-ras, which is already expressed in all tested tissues from control animals, is stimulated by clofibrate and ciprofibrate treatments. Comparatively these compounds stimulate the cyan…

MaleSomatic cellGenes mycBiophysicsBiologyKidneyMicrobodiesBiochemistryClofibric AcidProto-OncogenesmedicineAnimalsAcyl-CoA oxidaseClofibrateRNA MessengerMolecular BiologyHypolipidemic AgentsKidneyMessenger RNAClofibrateOncogeneFibric AcidsCell BiologyPeroxisomeMolecular biologyRats Inbred F344RatsGenes rasmedicine.anatomical_structureGene Expression RegulationLiverOrgan SpecificityAcyl-CoA OxidaseCiprofibrateOxidoreductasesmedicine.drugBiochemical and Biophysical Research Communications
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Fenofibrate effect on triglyceride and postprandial response of apolipoprotein A5 variants: the GOLDN study.

2007

Objective— Apolipoprotein A5 ( APOA5 ) is a key determinant of plasma triglyceride (TG) concentrations. Genetic variation at the APOA5 locus could be responsible for some of the observed differences in response to fenofibrate therapy. Methods and Results— We examined the association between tag SNPs (−1131T>C and 56C>G) at APOA5 and TG and HDL-C response to fenofibrate and a postprandial lipid challenge in 791 men and women participating in the GOLDN study. After 3-week drug treatment, APOA5 56G carriers displayed significant decrease in TG ( P =0.006), and increase in HDL-C ( P =0.002) levels relative to their basal values in the fasting state when compared with noncarriers (a TG re…

MaleTime FactorsApolipoprotein BAdministration Oralchemistry.chemical_compoundFenofibrateGene FrequencyApolipoprotein a5Hypolipidemic AgentsAged 80 and overFenofibratebiologyMiddle AgedPostprandial PeriodPostprandialTreatment OutcomeArea Under CurveFemaleCardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtyGuanineAdolescentGenotypeSingle-nucleotide polymorphismHyperlipidemiasPolymorphism Single NucleotideCytosineInternal medicinemedicineHumansParticle SizeApolipoproteins ATriglyceridesAgedTriglyceridebusiness.industryCholesterolCholesterol HDLCholesterol LDLDrug interactionLipid MetabolismDietary FatsUnited StatesEndocrinologychemistryApolipoprotein A-Vbiology.proteinbusinessThymineArteriosclerosis, thrombosis, and vascular biology
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Fibrate induction of the adrenoleukodystrophy-related gene (ABCD2)

2001

X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease due to a defect in the ABCD1 (ALD) gene. ABCD1, and the two close homologues ABCD2 (ALDR) and ABCD3 (PMP70), are genes encoding ATP-binding cassette half-transporters of the peroxisomal membrane. As overexpression of the ABCD2 or ABCD3 gene can reverse the biochemical phenotype of X-ALD (reduced beta-oxidation of very-long-chain fatty acids), pharmacological induction of these partially redundant genes may represent a therapeutic approach to X-ALD. We previously reported that the ABCD2 and ABCD3 genes could be strongly induced by fibrates, which are hypolipidaemic drugs and peroxisome-proliferators in rodents. We provide e…

MaleTranscription GeneticMolecular Sequence DataResponse elementReceptors Cytoplasmic and NuclearATP-binding cassette transporterATP Binding Cassette Transporter Subfamily DBiochemistryMiceFenofibrateABCD3Sequence Homology Nucleic AcidABCD2medicineAnimalsHumansRats WistarAdrenoleukodystrophyPromoter Regions GeneticGeneHypolipidemic AgentsMice KnockoutBase SequencebiologyDNATransfectionPeroxisomemedicine.diseaseMolecular biologyRatsGene Expression Regulationbiology.proteinATP-Binding Cassette TransportersAdrenoleukodystrophyTranscription FactorsEuropean Journal of Biochemistry
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Difference between Guinea Pig and Rat in the Liver Peroxisomal Response to Equivalent Plasmatic Level of Ciprofibrate

1996

Abstract Guinea pig was previously classified as a species nonresponsive to peroxisome proliferators. However, none of the previous reports was based on pharmacokinetic data. Here, after a comparative pharmacokinetic study between guinea pig and rat, we evaluate the guinea pig liver peroxisomal response to ciprofibrate, a hypolipemic agent and a potent peroxisome proliferator in rat. (1) Pharmacokinetic results show that plasmatic concentrations of ciprofibrate are equivalent in guinea pig and rat when guinea pigs are treated with ciprofibrate at 30 mg/kg twice a day and rats are treated at 3 mg/kg once a day. (2) The treatment of guinea pigs at 30 mg/kg twice a day for 2 weeks leads to a s…

Malemedicine.medical_specialtyGuinea PigsBiophysicsGene ExpressionPeroxisome ProliferationBiologyCell FractionationMicrobodiesBiochemistryMixed Function OxygenasesGuinea pigClofibric AcidCytochrome P-450 Enzyme SystemSpecies SpecificityPharmacokineticsInternal medicinemedicineAnimalsRNA MessengerMolecular BiologyHypolipidemic AgentsMessenger RNAOxidase testFibric AcidsPeroxisomeBlotting NorthernRatsEndocrinologyLiverMicrosomeAcyl-CoA OxidaseCiprofibrateCytochrome P-450 CYP4ADNA ProbesOxidoreductasesmedicine.drugArchives of Biochemistry and Biophysics
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Prevalence and Determinants of the Use of Lipid-Lowering Agents in a Population of Older Hospitalized Patients: the Findings from the REPOSI (REgistr…

2017

BACKGROUND: Older patients are prone to multimorbidity and polypharmacy, with an inherent risk of adverse events and drug interactions. To the best of our knowledge, available information on the appropriateness of lipid-lowering treatment is extremely limited. AIM: The aim of the present study was to quantify and characterize lipid-lowering drug use in a population of complex in-hospital older patients. METHODS: We analyzed data from 87 units of internal medicine or geriatric medicine in the REPOSI (Registro Politerapie della Società Italiana di Medicina Interna) study, with reference to the 2010 and 2012 patient cohorts. Lipid-lowering drug use was closely correlated with the clinical prof…

Malemedicine.medical_specialtyLogistic ModelLipid-Lowering AgentsPopulationSocio-culturaleOlder Hospitalized Patients030204 cardiovascular system & hematologyGeriatrics and Gerontology; Pharmacology (medical)03 medical and health sciences0302 clinical medicineInternal medicine80 and overPrevalencemedicineHumansPharmacology (medical)030212 general & internal medicineMedical prescriptionIntensive care medicineOmega 3 fatty acideducationAdverse effectAgedHypolipidemic AgentsAged 80 and overPolypharmacyGeriatricseducation.field_of_studyHypolipidemic Agentbusiness.industryGeriatrics and Gerontology Pharmacology (medical)HospitalizationLogistic ModelsCohortPolypharmacyAged; Aged 80 and over; Female; Hospitalization; Humans; Hypolipidemic Agents; Logistic Models; Male; Polypharmacy; Prevalence; Geriatrics and Gerontology; Pharmacology (medical)FemaleGeriatrics and GerontologybusinessAged; Aged 80 and over; Female; Hospitalization; Humans; Hypolipidemic Agents; Logistic Models; Male; Polypharmacy; PrevalenceHumanCohort study
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