Search results for "CHOLESTEROL EFFLUX"

showing 7 items of 7 documents

eNOS Activation by HDL Is Impaired in Genetic CETP Deficiency.

2014

Mutations in the CETP gene resulting in defective CETP activity have been shown to cause remarkable elevations of plasma HDL-C levels, with the accumulation in plasma of large, buoyant HDL particles enriched in apolipoprotein E. Genetic CETP deficiency thus represents a unique tool to evaluate how structural alterations of HDL impact on HDL atheroprotective functions. Aim of the present study was to assess the ability of HDL obtained from CETP-deficient subjects to protect endothelial cells from the development of endothelial dysfunction. HDL isolated from one homozygous and seven heterozygous carriers of CETP null mutations were evaluated for their ability to down-regulate cytokine-induced…

Settore MED/09 - Medicina InternaCHOLESTEROL EFFLUXApolipoprotein BEpidemiologylcsh:MedicineANTIINFLAMMATORY PROPERTIESmedicine.disease_causeBiochemistryVascular Medicinechemistry.chemical_compoundHigh-density lipoproteinEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceMutationMultidisciplinarybiologyHomozygoteCETP; eNOS; HDL;NeurochemistryLipidsGenetic EpidemiologyeNOSlipids (amino acids peptides and proteins)AnatomyNeurochemicalsLipoproteins HDLResearch Articlemedicine.medical_specialtyDrug Research and DevelopmentHDLNitric Oxide Synthase Type IIILipoproteinsENDOTHELIAL FUNCTIONINHIBITIONCardiologyDown-RegulationVascular Cell Adhesion Molecule-1Nitric OxideCELL-ADHESION MOLECULE-1Lipid Metabolism Inborn ErrorsESTER TRANSFER PROTEINInternal medicineCETPCholesterylester transfer proteinHuman Umbilical Vein Endothelial CellsmedicineHumansNITRIC-OXIDE SYNTHASEInflammationClinical GeneticsPharmacologyCholesterollcsh:RTorcetrapibEndothelial CellsBiology and Life SciencesProteinsnutritional and metabolic diseasesLipid MetabolismAtherosclerosismedicine.diseasebiology.organism_classificationCholesterol Ester Transfer Proteinscarbohydrates (lipids)MetabolismEndocrinologychemistryOther Clinical MedicineMutationImmunologyCardiovascular Anatomybiology.proteinlcsh:QTORCETRAPIBClinical MedicineHIGH-DENSITY-LIPOPROTEINSCAVENGER RECEPTOR BI
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Anti-Atherosclerotic Effect of a Polyphenol-Rich Ingredient, Oleactiv

2018

The development of nutraceutical ingredients has risen as a nutritional solution for health prevention. This study evaluated the effects of Oleactiv®, an ingredient developed for the prevention of atherogenesis, in hypercholesterolemic hamsters. Oleactiv® is a polyphenol-rich ingredient obtained from artichoke, olive and grape extracts as part of fruit and vegetables commonly consumed within the Mediterranean diet. A total of 21 Golden Syrian hamsters were divided into three groups. The standard group (STD) was fed a normolipidemic diet for 12 weeks, while the control group (CTRL) and Oleactiv® goup (OLE) were fed a high-fat diet. After sacrifice, the aortic fatty streak area (AFSA), plasma…

MaleHypercholesterolemiaAortic DiseasesAorta ThoracicDiet High-FatArticleCell LineoliveMiceAnimalsatheroma plaqueTriglyceridesMesocricetusAnticholesteremic AgentsMacrophagesCholesterol HDLhigh fat dietPolyphenolsAtherosclerosisgrapePlaque Atheroscleroticcholesterol efflux capacityreverse cholesterol transportDisease Models AnimalpolyphenolCholesterolDietary Supplementsaortic fatty streakartichokeNutrients
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Lack of Correlation of Plasma HDL With Fecal Cholesterol and Plasma Cholesterol Efflux Capacity Suggests Importance of HDL Functionality in Attenuati…

2018

A number of clinical findings suggested HDL-raising as a plausible approach to treat residual risk of CVD. However, lack of CVD risk reduction by elevated HDL cholesterol (HDL-C) through cholesterol ester transfer protein (CETP) inhibition and enhanced risk reduction in apolipoprotein A-I Milano (apoAI-M) individuals with low HDL-C shifted the focus from HDL-C level to HDL function. In the present study, we investigated correlations between HDL-C, HDL function, fecal cholesterol excretion, and ex vivo plasma cholesterol efflux capacity (CEC) in animal models using two HDL modulators, LXR and PPAR-α agonists. In C57Bl mice, LXR agonist, T1317, raised HDL-C by 30%, while PPAR-α agonist, fenof…

0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaHDLApolipoprotein BPhysiology030204 cardiovascular system & hematologylcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)Internal medicineCholesterylester transfer proteinmedicineHDL mouse PPAR-α LXR reverse cholesterol transport cholesterol efflux ABCA1 atherosclerosisLiver X receptormouseFenofibratelcsh:QP1-981biologyCholesterolReverse cholesterol transportnutritional and metabolic diseasesreverse cholesterol transport030104 developmental biologyEndocrinologychemistryABCA1biology.proteinCholesteryl esterLXRlipids (amino acids peptides and proteins)cholesterol effluxPPAR-αmedicine.drug
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Lomitapide affects HDL composition and function

2016

Abstract Background Lomitapide reduces low-density lipoprotein-cholesterol (LDL-C) but also high-density lipoprotein-cholesterol (HDL-C) levels. The latter may reduce the clinical efficacy of lomitapide. We investigated the effect of lomitapide on HDL-C levels and on cholesterol efflux capacity (CEC) of HDL in patients with homozygous familial hypercholesterolemia (HoFH). Methods and results Four HoFH patients were treated with increasing dosages of lomitapide. Lomitapide decreased LDL-C (range −34 to −89%). Total HDL-C levels decreased (range −16 to −34%) with a shift to buoyant HDL. ABCA1-mediated CEC decreased in all patients (range −39 to −99%). The changes of total, ABCG1- and SR-BI-me…

AdultMale0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaHDLHomozygous familial hypercholesterolemiaFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type IIYoung Adult03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineHumansMedicineIn patientClinical efficacyHyperlipoproteinemia Type IICholesterolbusiness.industryCholesterol HDLHomozygotenutritional and metabolic diseasesCholesterol LDLCholesterol efflux capacityAtherosclerosismedicine.diseaseCholesterol lowering drugsLomitapideLomitapideCholesterolPhenotypeTreatment Outcome030104 developmental biologyEndocrinologychemistryBenzimidazolesFemalelipids (amino acids peptides and proteins)Composition (visual arts)Cholesterol lowering drugHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins HDLCardiology and Cardiovascular MedicinebusinessATP Binding Cassette Transporter 1Atherosclerosis
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Effects of PCSK9 inhibitors on HDL cholesterol efflux and serum cholesterol loading capacity in familial hypercholesterolemia subjects: a multi-lipid…

2022

Proprotein convertase subtilisin/kexin type 9 (PCSK9), beyond regulating LDL cholesterol (LDL-c) plasma levels, exerts several pleiotropic effects by modulating lipid metabolism in extrahepatic cells such as macrophages. Macrophage cholesterol homeostasis depends on serum lipoprotein functions, including the HDL capacity to promote cell cholesterol efflux (CEC) and the serum capacity to promote cell cholesterol loading (CLC). The aim of this observational study was to investigate the effect of PCSK9 inhibitors (PCSK9-i) treatment on HDL-CEC and serum CLC in patients with familial hypercholesterolemia (FH). 31 genetically confirmed FH patients were recruited. Blood was collected and serum is…

cardiovascular riskSettore MED/09 - Medicina Internafamilial hypercholesterolemiaPCSK9 inhibitors cardiovascular risk cholesterol efflux capacity cholesterol loading capacity familial hypercholesterolemiaPCSK9 inhibitorsSettore BIO/14 - Farmacologiacholesterol loading capacityBiochemistry Genetics and Molecular Biology (miscellaneous)Molecular BiologyBiochemistrycholesterol efflux capacityPCSK9 inhibitors; cardiovascular risk; cholesterol efflux capacity; cholesterol loading capacity; familial hypercholesterolemiaFrontiers in molecular biosciences
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Exercise Training Favorably Modulates Gene and Protein Expression That Regulate Arterial Cholesterol Content in CETP Transgenic Mice

2018

Aerobic exercise training (AET) improves the reverse cholesterol transport (RCT) in cholesteryl ester transfer protein-transgenic (CETP-tg) mice. We aimed at investigating the role of AET in the expression of genes and proteins involved in lipid flux in the aorta and macrophages of CETP-tg mice. Three-month-old male mice were randomly divided into trained (T; treadmill 15 m/min; 30 min/day) and sedentary (S) groups. After 6 weeks, peritoneal macrophages and the aortic arch were obtained immediately (0 h) or 48 h after the last exercise session. mRNA was determined by RT-qPCR, protein levels by immunoblot and 14C-cholesterol efflux determined in macrophages. AET did not change body weight, p…

0301 basic medicinemedicine.medical_specialtyPhysiologymacrophage cholesterol effluxPeroxisome proliferator-activated receptor030204 cardiovascular system & hematologylcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinecholesterol ester transfer proteinPhysiology (medical)Internal medicineGene expressionCholesterylester transfer proteinmedicineAerobic exerciseOriginal Researchchemistry.chemical_classificationlcsh:QP1-981biologyCholesterolReverse cholesterol transportreverse cholesterol transport030104 developmental biologyEndocrinologychemistrybiology.proteinCholesteryl esterTERAPIA POR EXERCÍCIOlipids (amino acids peptides and proteins)Tumor necrosis factor alphaatherosclerosisexercise training
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Plasma and fibroblasts of Tangier disease patients are disturbed in transferring phospholipids onto apolipoprotein A-I

1998

Plasmas of patients with Tangier disease (TD) lack lipid-rich α-HDL which, in normal plasma, constitutes the majority of high density lipoprotein (HDL). Residual amounts of apolipoprotein (apo)A-I in TD plasma occur as lipid-poor or even lipid-free preβ-HDL. By contrast to normal plasma, TD plasma does not convert preβ-HDL into α-HDL. Moreover, fibroblasts of TD patients were found to be defective in secreting cholesterol or phospholipids in the presence of lipid-free apoA-I. We have therefore hypothesized that both defective conversion of preβ-HDL into α-HDL and defective lipid efflux from TD cells onto lipid-free apoA-I result from a disturbance in phospholipid transfer occurring in both …

AdultMaletransferring phospholipidsPhospholipidTangier diseasePhosphatidic AcidsQD415-436PhosphatidylinositolsBiochemistrychemistry.chemical_compoundEndocrinologyTangier diseasePhosphatidylcholinePhospholipid transfer proteinExtracellularmedicineHumansCells CulturedPhosphatidylethanolamineApolipoprotein A-ICholesterolPhosphatidylethanolaminesReverse cholesterol transportnutritional and metabolic diseasesBiological TransportCell BiologyFibroblastsmedicine.diseaseMolecular biologyfamilial HDL deficiencyreverse cholesterol transportLipoproteins LDLphospholipid transfer proteinsprebeta-HDLTangier disease; transferring phospholipidschemistryPhosphatidylcholinesFemalelipids (amino acids peptides and proteins)cholesterol efflux
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