Search results for "acids"

showing 10 items of 3520 documents

Lipids, Lipoproteins and Apolipoproteins A<sub>I</sub> A<sub>II</sub>, B, C<sub>II</sub>, C<sub>III</sub…

1991

In this study lipid and apolipoprotein patterns were investigated at birth and compared with those of adults. In cord sera, cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol were 38.2, 46.2, 50.5, and 31.9%, respectively, of adult values. Apolipoprotein A<sub>II</sub>, B and C<sub>III</sub> were 48.6, 30.6 and 44.5% of adult values, while apo A<sub>I</sub>, apo C<sub>II</sub> and apo E showed values approaching those of adults (63.4, 73.3 and 89.7%, respectively). Also cholesterol/HDL cholesterol and LDL cholesterol/HDL cholesterol ratios were lower in newborns. In cord sera, l…

Apolipoprotein ELdl cholesterolmedicine.medical_specialtyApolipoprotein BbiologyCholesterolLipid metabolismMetabolismPositive correlationchemistry.chemical_compoundEndocrinologychemistryInternal medicinePediatrics Perinatology and Child Healthmedicinebiology.proteinlipids (amino acids peptides and proteins)Developmental BiologyLipoproteinNeonatology
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Influence of microsomal triglyceride transfer protein promoter polymorphism -493 GT on fasting plasma triglyceride values and interaction with treatm…

2005

Familial hypercholesterolaemia (FH) is an autosomal dominant disease characterized by elevated levels of low-density lipoprotein-cholesterol (LDL-C). Phenotypic expression is highly variable, being influenced by diet, age, gender, body mass index, apolipoprotein E genotype and type of LDL-receptor gene mutation. Microsomal triglyceride (TG) transfer protein (MTP) is a protein involved in lipid metabolism. Polymorphism MTP -493 GT has been shown to modulate lipid levels in several populations. To analyse the effect of this polymorphism in the lipid phenotype expression of FH and treatment response, we studied a sample of 222 Spanish FH patients, of whom 147 were studied before and after trea…

Apolipoprotein EMaleAtorvastatinPolymerase Chain ReactionMicrosomal triglyceride transfer proteinBody Mass Indexchemistry.chemical_compoundAtorvastatinGeneral Pharmacology Toxicology and PharmaceuticsPromoter Regions GeneticGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsbiologyAutosomal dominant traitFastingLipoproteins LDLCholesterolPhenotypeMolecular Medicinelipids (amino acids peptides and proteins)Femalemedicine.drugmedicine.medical_specialtyHeterozygoteGenotypeLipoproteinsHyperlipoproteinemia Type IIApolipoproteins ESex FactorsInternal medicineGeneticsmedicineHumansPyrrolesMolecular BiologyAllelesTriglyceridesPolymorphism GeneticTriglycerideCholesterolGenetic VariationCholesterol LDLDNALipid MetabolismEndocrinologychemistryHeptanoic AcidsPharmacogeneticsMutationbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsCarrier ProteinsBody mass indexPharmacogeneticsPharmacogenetics and genomics
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Haptoglobin interacts with apolipoprotein E and beta-amyloid and influences their crosstalk.

2014

Beta-amyloid accumulation in brain is a driving force for Alzheimer's disease pathogenesis. Apolipoprotein E (ApoE) represents a critical player in beta-amyloid homeostasis, but its role in disease progression is controversial. We previously reported that the acute-phase protein haptoglobin binds ApoE and impairs its function in cholesterol homeostasis. The major aims of this study were to characterize the binding of haptoglobin to beta-amyloid, and to evaluate whether haptoglobin affects ApoE binding to beta-amyloid. Haptoglobin is here reported to form a complex with beta-amyloid as shown by immunoblotting experiments with purified proteins, or by its immunoprecipitation in brain tissues …

Apolipoprotein EMalePhysiologyDiseaseBeta-amyloidBiochemistryAmyloid beta-Protein PrecursorAlzheimer' diseasepolycyclic compoundsskin and connective tissue diseasesapolipoprotein EbiologyChemistryMedicine (all)Haptoglobinfood and beveragesBrainApoE/A? complexGeneral MedicineMiddle AgedhaptoglobinCrosstalk (biology)ApoE/Aβ complexSettore MED/26 - Neurologialipids (amino acids peptides and proteins)FemaleAlzheimer's diseaseProtein BindingAdultmedicine.medical_specialtyImmunoprecipitationCognitive NeuroscienceEnzyme-Linked Immunosorbent AssayCHO CellsTransfectionAlzheimer' disease; ApoE/Aβ complex; Apolipoprotein E; Beta-amyloid; Haptoglobin; Human brain tissue; Adult; Aged; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Analysis of Variance; Animals; Apolipoproteins E; Brain; CHO Cells; Cricetulus; Enzyme-Linked Immunosorbent Assay; Female; Haptoglobins; Humans; Immunoprecipitation; Male; Middle Aged; Mutation; Protein Binding; Transfection; Biochemistry; Cell Biology; Physiology; Cognitive Neuroscience; Medicine (all)NOApolipoproteins ECricetulusAlzheimer DiseaseInternal medicinemental disordersmedicineAnimalsHumansImmunoprecipitationAgedAnalysis of VarianceAmyloid beta-PeptidesHaptoglobinsNeurotoxicityAlzheimer’diseaseCell Biologymedicine.diseasehuman brain tissueEndocrinologyMutationbiology.proteinAlzheimer'diseaseHomeostasisACS chemical neuroscience
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The relationship between cortisol and cognitive function in healthy older people: The moderating role of Apolipoprotein E polymorphism.

2018

The Apolipoprotein E4 (ApoE-epsilon 4) allele has been suggested as the main risk factor for late onset Alzheimer's disease (AD), whereas the ApoE-epsilon 2 allele has been proposed as a protective factor. These proposals have increased the interest in the effect of the ApoE genotype in healthy people. Additionally, high cortisol levels have been related to negative effects on cognition. However, few studies have investigated the relationship between cognitive performance and cortisol, taking into account the different ApoE alleles. For this reason, the aim of this study was to evaluate different cognitive domains (declarative and working memory, attention, and executive function) and their…

Apolipoprotein EMaleSALIVARY CORTISOLHydrocortisonePituitary-Adrenal SystemCortisolBehavioral NeuroscienceExecutive FunctionPOSTTRAUMATIC-STRESS-DISORDER0302 clinical medicineCognitionGenotypeSOCIOECONOMIC-STATUSAttentionPOPULATIONeducation.field_of_study05 social sciencesNeuropsychologyCognitionMiddle AgedALZHEIMERS-DISEASElipids (amino acids peptides and proteins)FemaleApolipoprotein Emedicine.medical_specialtyHypothalamo-Hypophyseal SystemSEX-DIFFERENCESCognitive NeurosciencePopulationExperimental and Cognitive PsychologyPolymorphism Single Nucleotide050105 experimental psychology03 medical and health sciencesApolipoproteins EMemoryAWAKENING RESPONSEInternal medicinemedicineHumans0501 psychology and cognitive sciencesEffects of sleep deprivation on cognitive performanceAlleleeducationAgedELDERLYWorking memorybusiness.industryMEMORY PERFORMANCEE GENOTYPEBODY-MASS INDEXEndocrinologyOlder peoplebusinessNeuroscience030217 neurology & neurosurgeryNeurobiology of learning and memory
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Genetic polymorphisms affecting the phenotypic expression in familial hypercholesterolemia

2004

The clinical expression of heterozygous familial hypercholesterolemia (FH) is highly variable even in patients carrying the same LDL receptor (LDL-R) gene mutation. This variability might be due to environmental factors as well as to modifying genes affecting lipoprotein metabolism. We investigated Apo E (2, 3, 4), MTP (-493G/T), Apo B (-516C/T), Apo A-V (-1131T/C), HL (-514C/T and -250G/A), FABP-2 (A54T), LPL (D9N, N291S, S447X) and ABCA1 (R219K) polymorphisms in 221 unrelated FH index cases and 349 FH relatives with defined LDL-R gene mutations. We found a significant and independent effect of the following polymorphisms on: (i) plasma LDL-C (Apo E, MTP and Apo B); (ii) plasma HDL-C (HL, …

Apolipoprotein EMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemiaGene mutationPolymerase Chain ReactionCoronary artery diseasecoronary artery disease; familial hypercholesterolemia; genetic polymorphisms; plasma lipidsCohort Studieschemistry.chemical_compoundGenotypePlasma lipidsOdds RatiobiologyFamilial hypercholesterolemia Plasma lipids Genetic polymorphisms Coronary artery diseaseIncidenceMiddle AgedPhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyMolecular Sequence DataFamilial hypercholesterolemiaPlasma lipidGenetic polymorphismsRisk AssessmentHyperlipoproteinemia Type IIFamilial hypercholesterolemia; Plasma lipids; Genetic polymorphisms; Coronary artery diseasePredictive Value of TestsInternal medicinemedicineConfidence IntervalsHumansGenetic Predisposition to DiseaseGenetic polymorphismPolymorphism GeneticBase SequenceCholesterolCholesterol HDLCase-control studyCholesterol LDLmedicine.diseaseEndocrinologyApolipoproteinschemistrySettore MED/03 - Genetica MedicaGene Expression RegulationReceptors LDLCase-Control StudiesLDL receptorbiology.protein
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Estrogen up-regulates apolipoprotein E (ApoE) gene expression by increasing ApoE mRNA in the translating pool via the estrogen receptor alpha-mediate…

1998

The antiatherogenic property of estrogens is mediated via at least two mechanisms: first by affecting plasma lipoprotein profiles, and second by affecting the components of the vessel wall. Raising plasma apolipoprotein E (apoE) in mice protects them against diet-induced atherosclerosis (Shimano, H., Yamada, N., Katsuki, M., Gotoda, T., Harada, K., Murase, T., Fukuzawa, C., Takaku, F., and Yazaka, Y. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 1750-1754). It is possible that estrogen may be antiatherogenic at least in part by increasing plasma apoE levels. Therefore, we studied the regulation of apoE by estrogen. A survey of 15 inbred strains of mice showed that some mouse strains responded …

Apolipoprotein EMalemedicine.medical_specialtyApolipoprotein Bmedicine.drug_classEstrogen receptorBiochemistrychemistry.chemical_compoundMiceHigh-density lipoproteinApolipoproteins EInternal medicinemedicineAnimalsRNA MessengerReceptorMolecular BiologyMice Inbred BALB CMice Inbred C3HbiologyEstradiolEstrogen Receptor alphaCell BiologyLipidsUp-RegulationMice Inbred C57BLEndocrinologychemistryGene Expression RegulationLiverReceptors EstrogenEstrogenbiology.proteinlipids (amino acids peptides and proteins)Estrogen receptor alphaLipoproteinThe Journal of biological chemistry
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Serum lipid responses to phytosterol-enriched milk in a moderate hypercholesterolemic population is not affected by apolipoprotein E polymorphism or …

2011

Background/Objectives: The importance of both low-density lipoprotein cholesterol (LDLc) size and the apolipoprotein E (Apo E) in the atherogenic process is known, but there is little information with regard to the effect of phytosterols (PS) on these parameters. The aim of this study was to evaluate the influence of PS on lipid profile and LDLc size according to Apo E genotype. Subjects/Methods: This was a randomized parallel trial employing 75 mild-hypercholesterolemic subjects and consisting of two 3-month intervention phases. After 3 months of receiving a standard healthy diet, subjects were divided into two intervention groups: a diet group (n = 34) and a diet+PS group (n = 41) that re…

Apolipoprotein EMalemedicine.medical_specialtyGenotype030309 nutrition & dieteticsPopulationHypercholesterolemiaMedicine (miscellaneous)030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineApolipoproteins EDouble-Blind MethodInternal medicineHyperlipidemiamedicineAnimalsHumansParticle SizeeducationApolipoprotein e polymorphismTriglycerides0303 health scienceseducation.field_of_studyNutrition and DieteticsPolymorphism GeneticCholesterolPhytosterolCholesterol HDLPhytosterolsCholesterol LDLMiddle Agedmedicine.diseaseLipidsLipoproteins LDLEndocrinologyCholesterolMilkTreatment OutcomechemistryLow-density lipoproteinFood FortifiedFemalelipids (amino acids peptides and proteins)Lipoprotein
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Effects of PCSK9 variants on common carotid artery intima media thickness and relation to ApoE alleles.

2009

BACKGROUND: PCSK9 plays a key role in plasma cholesterol metabolism by modulating the expression of LDL receptors. OBJECTIVE AND METHODS: In this study we investigated the effects of two common polymorphism of the PCSK9 gene (E670G and I474V) on the intima media thickness of the common carotid artery and the possible relation with polymorphisms of apolipoprotein E in 1541 middle aged subjects selected from the general population enrolled in the PLIC study and confirmed the major findings in a second free-living population enrolled in the Ventimiglia study. RESULTS: 670G carriers showed significantly increased plasma total cholesterol, LDL-cholesterol, and Apo levels B while no significant d…

Apolipoprotein EMalemedicine.medical_specialtyPathologySettore MED/09 - Medicina InternaCarotid Artery CommonPopulationBiologyPCSK9PCSK9 GeneApolipoproteins Emedicine.arteryInternal medicinemedicineHumansCommon carotid arteryAlleleeducationAlleleseducation.field_of_studyIn silico modelingPolymorphism GeneticIMTPCSK9Serine EndopeptidasesMiddle AgedEndocrinologyIntima-media thicknessLDL receptorlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesMolecular geneticProprotein Convertase 9Cardiology and Cardiovascular MedicineTunica IntimaTunica MediaAtherosclerosis
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Overexpression of human hepatic lipase and ApoE in transgenic rabbits attenuates response to dietary cholesterol and alters lipoprotein subclass dist…

1999

Abstract —The effect of the expression of human hepatic lipase (HL) or human apoE on plasma lipoproteins in transgenic rabbits in response to dietary cholesterol was compared with the response of nontransgenic control rabbits. Supplementation of a chow diet with 0.3% cholesterol and 3.0% soybean oil for 10 weeks resulted in markedly increased levels of plasma cholesterol and VLDL and IDL in control rabbits as expected. Expression of either HL or apoE reduced plasma cholesterol response by 75% and 60%, respectively. The HL transgenic rabbits had substantial reductions in medium and small VLDL and IDL fractions but not in larger VLDL. LDL levels were also reduced, with a shift from larger, m…

Apolipoprotein EMalemedicine.medical_specialtyVery low-density lipoproteinTransgeneLipoproteinsCholesterol VLDLHypercholesterolemiaGene ExpressionPathogenesisAnimals Genetically ModifiedCholesterol Dietarychemistry.chemical_compoundApolipoproteins EInternal medicinemedicineAnimalsHumansTransgenesParticle SizeApolipoproteins BLagomorphabiologyCholesterolCholesterol HDLLipasebiology.organism_classificationEndocrinologyCholesterolchemistrylipoproteins apoE hepatic lipase rabbits transgeneLiverDiet Atherogeniclipids (amino acids peptides and proteins)Hepatic lipaseRabbitsCardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Increased Atherosclerotic Lesions in ApoE Mice With Plasma Phospholipid Transfer Protein Overexpression

2003

Objective— Plasma phospholipid transfer protein (PLTP) is involved in the metabolism of HDL and apolipoprotein B (apoB)-containing lipoproteins. Atherosclerosis susceptibility is decreased in mice with PLTP deficiency that is associated with decreased liver production of apoB-containing lipoproteins and increase in their antioxidant. To investigate additionally the effect of PLTP on the development of atherosclerosis, we overexpressed PLTP in mice. Methods and Results— PLTP was overexpressed in apoE knockout mice using an adenovirus-associated virus (AAV)-mediated system. Plasma PLTP activity was 1.3- to 2-fold higher in mice injected with AAV-PLTP than in mice injected with control AAV-GF…

Apolipoprotein Emedicine.medical_specialtyApolipoprotein BArteriosclerosisLipoproteinsmedicine.medical_treatmentGenetic Vectorsalpha-TocopherolPhospholipidAdenoviridaeInjectionsMicechemistry.chemical_compoundApolipoproteins EHigh-density lipoproteinPhospholipid transfer proteinInternal medicinemedicineAnimalsPhospholipid Transfer ProteinsbiologyCholesterolVitamin EMembrane ProteinsLipidsMice Inbred C57BLEndocrinologychemistrybiology.proteinFemalelipids (amino acids peptides and proteins)Carrier ProteinsCardiology and Cardiovascular MedicineOxidation-ReductionLipoproteinArteriosclerosis, Thrombosis, and Vascular Biology
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