Search results for "apolipoprotein"

showing 10 items of 354 documents

Influence of genetic variation at the apo A-I gene locus on lipid levels and response to diet in familial hypercholesterolemia

1998

We have examined the apo AI - 75 (G/A) and apo AI + 83(MspI +/-) polymorphisms at the APOA1 gene locus for associations with plasma lipid levels and response to an NCEP-I diet in 69 (44 women, 25 men) heterozygotes for familial hypercholesterolemia (FH). Subjects were studied at baseline (after consuming for one month a diet with 35%, fat, 10% saturated, and 300 mg/day cholesterol) and after 3 months of an NCEP-I diet. No gender-related differences for any of the lipid variables examined were found and the data were analyzed for men and women combined. For the apo AI - 75 (G/A) polymorphism, there were 51 G/G and 18 G/A subjects. At baseline, G/A subjects showed significantly lower total ch…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BCholesterol VLDLLocus (genetics)Familial hypercholesterolemiaHyperlipoproteinemia Type IIchemistry.chemical_compoundInternal medicineGenetic variationAPOA1 GenemedicineHumansAlleleAllelesGeneticsPolymorphism GeneticApolipoprotein A-IbiologyCholesterolCholesterol HDLGenetic VariationHeterozygote advantageCholesterol LDLmedicine.diseaseLipidsDietEndocrinologychemistrybiology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAtherosclerosis
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Evaluation of clinical diagnosis criteria of familial ligand defective apoB 100 and lipoprotein phenotype comparison between LDL receptor gene mutati…

2007

Familial hypercholesterolemia (FH) and familial defective apoB 100 (FDB) are characterized by increased plasma low-density lipoprotein cholesterol (LDLc) levels and risk of coronary heart disease (CHD). FDB is clinically indistinguishable from FH. The aims of this study were to evaluate clinical diagnosis criteria for FDB and to compare the lipoprotein phenotype between carriers of LDL receptor (LDLR) gene mutations that affect the ligand-binding domain and subjects with the R3500Q mutation in apoB gene. We studied 213 subjects (113 probands) with FH and 19 heterozygous FDB subjects. Genetic diagnosis was determined by following a protocol based on Southern blot and polymerase chain reactio…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BPopulationMutation MissenseCoronary DiseaseFamilial hypercholesterolemiaGene mutationBiologyWhite PeopleHyperlipoproteinemia Type IIchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansMissense mutationeducationPolymorphism Single-Stranded Conformationaleducation.field_of_studyBinding SitesCholesterolGenetic Carrier ScreeningBiochemistry (medical)Public Health Environmental and Occupational HealthCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseFounder EffectProtein Structure TertiaryEuropePhenotypeEndocrinologyReceptors LDLchemistryApolipoprotein B-100LDL receptorbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinTranslational Research
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Genetic Variation at the ApoA-IV Gene Locus and Response to Diet in Familial Hypercholesterolemia

1998

Abstract —Plasma lipid response to dietary fat and cholesterol is, in part, genetically controlled. The apolipoprotein A-IV (apoA-IV protein; APOA4, gene) has been shown to influence the response to dietary changes in normolipidemic individuals. The response to diet in subjects with familial hypercholesterolemia (FH) is also variable, and no studies are available on the influence of APOA4 mutations on dietary response in these subjects. We studied the effect of 2 common apoA-IV genetic variants (Gln 360 →His and Thr 347 →Ser) on the lipid response to the National Cholesterol Education Program type I (NCEP-I) diet in 67 FH heterozygotes (43 women and 24 men). Subjects were studied at baseli…

AdultMaleHeterozygotemedicine.medical_specialtyVery low-density lipoproteinGenotypeApolipoprotein BHypercholesterolemiaFamilial hypercholesterolemiaStatistics Nonparametricchemistry.chemical_compoundHigh-density lipoproteinInternal medicinemedicineHumansAlleleNational Cholesterol Education ProgramAllelesApolipoproteins AGeneticsAnalysis of VariancebiologyCholesterolGenetic VariationMiddle Agedmedicine.diseaseDietary FatsLipidsEndocrinologychemistryLow-density lipoproteinMutationbiology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineArteriosclerosis, Thrombosis, and Vascular Biology
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Gemfibrozil reduces small low-density lipoprotein more in normolipemic subjects classified as low-density lipoprotein pattern B compared with pattern…

2005

We tested the hypothesis that gemfibrozil has a differential effect on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subclass distributions and postprandial lipemia that is different in subjects classified as having LDL subclass pattern A or LDL pattern B who do not have a classic lipid disorder. Forty-three normolipemic subjects were randomized to gemfibrozil (1,200 mg/day) or placebo for 12 weeks. Lipids and lipoproteins were determined by enzymatic methods. The mass concentrations of lipoproteins in plasma were determined by analytic ultracentrifugation and included the S(f) intervals: 20 to 400 (very LDL), 12 to 20 (intermediate-density lipoprotein), 0 to 12 (LDL), an…

AdultMaleHyperlipoproteinemiasmedicine.medical_specialtySmall dense ldlLipid disorderApolipoprotein BLipoproteins VLDLPlacebochemistry.chemical_compoundDouble-Blind MethodInternal medicinemedicineHumansGemfibrozilTriglyceridesAgedHypolipidemic Agentsbiologybusiness.industryMiddle AgedPostprandial PeriodLipoproteins LDLTreatment OutcomeEndocrinologyPostprandialchemistryLow-density lipoproteinbiology.proteinFemalelipids (amino acids peptides and proteins)GemfibrozilLipoproteins HDLCardiology and Cardiovascular MedicinebusinessGemfibrozil small low-density lipoprotein pattern B pattern ABiomarkersLipoproteinmedicine.drug
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G×E Interaction Influences Trajectories of Hand Grip Strength.

2016

Age-related decline in grip strength predicts later life disability, frailty, lower well-being and cognitive change. While grip strength is heritable, genetic influence on change in grip strength has been relatively ignored, with non-shared environmental influence identified as the primary contributor in a single longitudinal study. The extent to which gene-environment interplay, particularly gene-environment interactions, contributes to grip trajectories has yet to be examined. We considered longitudinal grip strength measurements in seven twin studies of aging in the Interplay of Genes and Environment across Multiple Studies consortium. Growth curve parameters were estimated for same-sex …

AdultMaleLongitudinal studyAgingTwinsTwins Monozygotic/geneticsBiologyEnvironmentArticle03 medical and health sciencesGrip strength0302 clinical medicineApolipoproteins ECognitive changeHand strengthGeneticsHumans030212 general & internal medicineHand Strength/physiologyAging/psychologyLongitudinal StudiesGene–environment interactionGenetics (clinical)Ecology Evolution Behavior and SystematicsAgedAged 80 and overHand StrengthAge FactorsGrowth curve (biology)Twins MonozygoticMiddle AgedTwin studyGene-environment interactionkaksosetGrip strengthFemaleGene-Environment InteractionApolipoproteins E/genetics030217 neurology & neurosurgeryAPOEDemographyBehavior genetics
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Associations of Aerobic Fitness and Maximal Muscular Strength With Metabolites in Young Men

2019

This cross-sectional study of young Finnish men examines the associations of aerobic fitness and muscular strength with metabolome measures that are associated with cardiometabolic risks.

AdultMalePhysical fitnessCardiologyPhysiologyPhysical strengthBody fat percentageLipoprotein particlechemistry.chemical_compoundYoung AdultRisk FactorsMedicineAerobic exerciseHumansMuscle Strengthmetabolinen oireyhtymäExerciseFinlandOriginal Investigationaerobic fitnessmaximal muscular strengthTriglyceridebiologybusiness.industryResearchVO2 maxGeneral MedicineMiddle AgedOnline OnlyCross-Sectional StudiesMetabolismMilitary PersonnelchemistryPhysical Fitnessbiology.proteinsydän- ja verisuonitauditMetabolomeApolipoprotein A1aerobinen suorituskykybusinesslihaskuntoBiomarkerscardiometabolic disease riskJAMA Network Open
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Autosomal recessive hypercholesterolemia in a Sicilian kindred harboring the 432insA mutation of the ARH gene

2003

Abstract We describe a Sicilian family presenting a recessive form of hypercholesterolemia harboring a mutation of the autosomal recessive hypercholesterolemia (ARH) gene. In two of the three sibs, a 26-year-old male and a 22-year-old female, a severe hypercholesterolemia was diagnosed with very high levels of plasma cholesterol (15.9 and 12.2 mmol/l, respectively); tendon xanthomatas and xanthelasms were present and in the male proband was documented a diffuse coronary atherosclerotic disease with a rapid and fatal progression. Both the parents had normal or slightly increased levels of plasma cholesterol. All causes of secondary hypercholesterolemia were ruled out as well as an involvemen…

AdultMaleProbandHeterozygotemedicine.medical_specialtyApolipoprotein BDNA Mutational AnalysisMolecular Sequence DataGenes RecessiveARH geneCoronary AngiographyRisk AssessmentGenetic determinismHyperlipoproteinemia Type IIInternal medicinemedicineHumansPoint MutationRNA MessengerSicilyGeneAdaptor Proteins Signal TransducingHypolipidemic AgentsGeneticsBase SequencebiologySiblingsCoronary StenosisHeterozygote advantageAutosomal recessive hypercholesterolemiaPedigreeAdaptor Proteins Vesicular TransportTreatment OutcomeEndocrinologyAutosomal Recessive HypercholesterolemiaMutationLDL receptorMutation (genetic algorithm)biology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFollow-Up StudiesAtherosclerosis
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Familial hypobetalipoproteinemia due to apolipoprotein B R463W mutation causes intestinal fat accumulation and low postprandial lipemia

2008

Abstract Objective Familial hypobetalipoproteinemia (FHBL) is characterized by inherited low plasma levels of apolipoprotein B (apoB)-containing lipoproteins. In this paper we investigated whether the already described APOB R463W missense mutation, a FHBL mutation able to impair the activity of microsomal triglyceride transfer protein (MTP), may cause intestinal fat accumulation and reduced postprandial lipemia. Methods Four out of five probands harboring APOB R463W mutation were compared with six healthy controls and six patients with celiac disease (CD). An oral fat load supplemented with retinyl palmitate (RP) was administered and a gastro-duodenal endoscopy with biopsy was performed. Re…

AdultMaleRetinyl Estersmedicine.medical_specialtySettore MED/09 - Medicina InternaAdolescentApolipoprotein BMutation MissenseapolipoproteinBlood lipidsHyperlipidemiasIntra-Abdominal FatBiologyMicrosomal triglyceride transfer proteinchemistry.chemical_compoundRetinyl palmitateInternal medicinemedicineHumansMissense mutationIntestinal MucosaChildVitamin ATriglyceridesApolipoproteins BTriglycerideMiddle AgedLipid MetabolismPostprandial Periodmedicine.diseasePostprandialEndocrinologychemistryHypobetalipoproteinemia Familial Apolipoprotein BB R463Wbiology.proteinFemalelipids (amino acids peptides and proteins)HypobetalipoproteinemiaDiterpenesCarrier ProteinsCardiology and Cardiovascular MedicineAtherosclerosis
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Low testosterone levels are related to oxidative stress, mitochondrial dysfunction and altered subclinical atherosclerotic markers in type 2 diabetic…

2017

Abstract Introduction Low testosterone levels in men are associated with type 2 diabetes and cardiovascular risk. However, the role of testosterone in mitochondrial function and leukocyte-endothelium interactions is unknown. Our aim was to evaluate the relationship between testosterone levels, metabolic parameters, oxidative stress, mitochondrial function, inflammation and leukocyte-endothelium interactions in type 2 diabetic patients. Materials and methods The study was performed in 280 male type 2 diabetic patients and 50 control subjects. Anthropometric and metabolic parameters, testosterone levels, reactive oxygen species (ROS) production, mitochondrial membrane potential, TNFα, adhesio…

AdultMaleRiskMitochondrial ROSmedicine.medical_specialtyApolipoprotein BVascular Cell Adhesion Molecule-1030209 endocrinology & metabolismInflammationType 2 diabetes030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineLeukocytesmedicineHumansTestosteroneMembrane Potential Mitochondrialchemistry.chemical_classificationReactive oxygen speciesbiologyTestosterone (patch)Middle AgedAtherosclerosismedicine.diseaseMitochondriaOxidative StressEndocrinologyDiabetes Mellitus Type 2chemistrybiology.proteinCytokinesInflammation Mediatorsmedicine.symptomReactive Oxygen SpeciesBiomarkersOxidative stressFree Radical Biology and Medicine
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Influence of the APOA5 locus on plasma triglyceride, lipoprotein subclasses, and CVD risk in the Framingham Heart Study

2004

Several polymorphisms in the APOA5 gene have been associated with increased plasma triglyceride (TG) concentrations. However, associations between APOA5 and lipoprotein subclasses, remnant-like particles (RLPs), and cardiovascular disease (CVD) risk have been less explored. We investigated associations of five APOA5 single-nucleotide polymorphisms (SNPs; −1131T>C, −3A>G, 56C>G IVS3+ 476G>A, and 1259T>C) with lipoprotein subfractions and CVD risk in 1,129 men and 1,262 women participating in the Framingham Heart Study. Except for the 56C>G SNP, the other SNPs were in significant linkage disequilibria, resulting in three haplotypes (11111, 22122, and 11211) representing 98% of the population.…

AdultMaleRiskhaplotypemedicine.medical_specialtyGenotypeLipoproteinsPopulationCoronary DiseaseSingle-nucleotide polymorphismQD415-436BiologyCardiovascular SystemPolymorphism Single NucleotideBiochemistryLinkage Disequilibriumchemistry.chemical_compoundSex FactorsEndocrinologyFramingham Heart StudyInternal medicineremnant-like particlesmedicineHumansSNPAlleleeducationAllelesApolipoproteins ATriglyceridesAgededucation.field_of_studyPolymorphism GeneticCholesterolHaplotypeGenetic VariationCell BiologyMiddle Agedcardiovascular disease riskApolipoproteinsCholesterolEndocrinologyHaplotypeschemistryApolipoprotein A-VCardiovascular DiseasesFemaleLipoproteinJournal of Lipid Research
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