Search results for "fibra"

showing 10 items of 172 documents

Differential regulation by a peroxisome proliferator of the different multifunctional proteins in guinea pig: cDNA cloning of the guinea pig D-specif…

1998

After our previous report on the cloning of two cDNA species in guinea pig, both encoding the same hepatic 79 kDa multifunctional protein 1 (MFP-1) [Caira, Cherkaoui-Malki, Hoefler and Latruffe (1996) FEBS Lett. 378, 57-60], here we report the cloning of a cDNA encoding a second multifunctional peroxisomal protein (MFP-2) in guinea-pig liver. This 2356 nt cDNA encodes a protein of 735 residues (79.7 kDa) whose sequence shows 83% identity with rat MFP-2 [Dieuaide-Noubhani, Novikov, Baumgart, Vanhooren, Fransen, Goethals, Vandekerckhove, Van Veldhoven and Mannaerts (1996) Eur. J. Biochem. 240, 660-666]. In parallel, we studied the effect of ciprofibrate, a hypolipaemic agent also known as per…

MaleDNA ComplementaryTranscription GeneticGuinea PigsMolecular Sequence DataBiologyMicrobodiesBiochemistryEstradiol DehydrogenasesRats Sprague-DawleyGuinea pigClofibric AcidComplementary DNAGene expressionmedicineAnimalsAmino Acid SequenceRNA MessengerNorthern blotCloning MolecularEnoyl-CoA HydrataseMolecular BiologyHypolipidemic AgentsMessenger RNABase SequenceThiolaseFibric AcidsCell BiologyPeroxisomeMolecular biologyRatsGene Expression RegulationLiverBiochemistryCiprofibrateOxidoreductasesResearch Articlemedicine.drugBiochemical Journal
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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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Copurification of dihydroxyacetone-phosphate acyl-transferase and other peroxisomal proteins from liver of fenofibrate-treated rats.

1997

Dihydroxyacetone-phosphate acyl-transferase (DHAP-AT), a peroxisomal membrane-bound enzyme that catalyzes the first step of ether-glycerolipid synthesis, was purified from liver of rats treated with fenofibrate, a peroxisome proliferator. The protocol first included isolation of peroxisomes, their purification through a discontinuous gradient and solubilization of membranes in CHAPS. DHAP-AT was further purified by four chromatographic steps, namely low-pressure size-exclusion, cation-exchange, hydroxylapatite and chromatofocusing. The chromatofocusing step led to a 4000-fold increase in the specific activity of DHAP-AT with respect to the liver homogenate with a yield of about 0.2%. Trypsi…

MaleMolecular Sequence DataBiochemistryMicrobodiesCopurificationchemistry.chemical_compoundFenofibrateProtein purificationAnimalsAmino Acid SequenceRats WistarPeptide sequenceDihydroxyacetone phosphatechemistry.chemical_classificationOxidase testChromatofocusingMembrane ProteinsGeneral MedicinePeroxisomeMolecular biologyRatsEnzymechemistryBiochemistryLiverSolubilitySequence AnalysisAcyltransferasesBiochimie
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Transcriptional induction of the fatty acid binding protein gene in mouse liver by bezafibrate

1993

AbstractThe mechanism by which hypolipidemic peroxisome proliferators of the fibrate family induce the liver fatty acid binding protein in liver of rodents is unknown. In order to delineate the level at which this protein is induced, the transcriptional activity of the specific gene encoding for liver fatty acid binding protein was measured in isolated hepatocyte nuclei obtained from male Swiss mice daily force-fed during 7 days with 400 mg/kg body weight bezafibrate. This treatment induced a 4-fold increase in the liver fatty acid binding protein transcription rate. Liver fatty acid binding protein mRNA level, measured by Northern blot analysis and cytosolic content of this protein, analyz…

MalePeroxisome proliferator activated receptorTranscription GeneticImmunoblottingBiophysicsPeroxisome proliferator-activated receptorNerve Tissue ProteinsFatty Acid-Binding ProteinsPeroxisome proliferator hypolipidemic drugBiochemistryFatty acid-binding proteinMiceStructural BiologyGeneticsmedicineAnimalsRNA Messengeradipocyte protein 2Molecular Biologychemistry.chemical_classificationLiver fatty acid binding proteinBezafibratebiologyBinding proteinBody WeightCell BiologyOrgan SizePeroxisomeBlotting NorthernMolecular biologyLipidsNeoplasm ProteinsGene regulationFatty acid synthasechemistryBiochemistryGene Expression RegulationLiverbiology.proteinElectrophoresis Polyacrylamide GelPeroxisome proliferator-activated receptor alphaBezafibrateCarrier ProteinsDNA ProbesFatty Acid-Binding Protein 7medicine.drugFEBS Letters
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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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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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