Search results for "Apolipoprotein B"

showing 10 items of 170 documents

Differential effects of oxidized LDL on apolipoprotein AI and B synthesis in HepG2 cells

2006

Oxidized low-density lipoproteins (Ox-LDL) are key elements in atherogenesis. Apolipoprotein AI (apoAI) is an active component of the antiatherogenic high-density lipoproteins (HDL). In contrast, plasma apolipoprotein B (apoB), the main component of LDL, is highly correlated with coronary risk. Our results, obtained in HepG2 cells, show that Ox-LDL, unlike native LDL, leads to opposite effects on apoB and apoAI, namely a decrease in apoAI and an increase in apoB secretion as evaluated by [(3)H]leucine incorporation and specific immunoprecipitation. Parallel pulse-chase studies show that Ox-LDL impaired apoB degradation, whereas apoAI degradation was increased and mRNA levels were decreased.…

medicine.medical_specialtyTime FactorsFree RadicalsApolipoprotein BImmunoprecipitationBiochemistryCell Linechemistry.chemical_compoundLeucinePhysiology (medical)Lipid biosynthesisInternal medicinemedicineHumansSecretionRNA MessengerTriglyceridesGlyceraldehyde 3-phosphate dehydrogenaseApolipoproteins BApolipoprotein A-IbiologyCholesterolnutritional and metabolic diseasesAtherosclerosisLipidsMOPSLipoproteins LDLOxygenEndocrinologychemistryCell culturebiology.proteinlipids (amino acids peptides and proteins)Cholesterol EstersFree Radical Biology and Medicine
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Changes in serum lipid and lipoprotein concentrations and compositions at birth and after 1 month of life in macrosomic infants of insulin-dependent …

1999

The aim of this study was to determine whether macrosomia related to maternal diabetes alters lipoprotein metabolism and whether these abnormalities still persist or regress after 1 month of life. Serum lipoprotein compositions and concentrations as well as serum lipid fatty acid compositions were investigated in macrosomic infants (birth weight = 4840 +/- 105 g at term) of insulin-dependent diabetic mothers at birth and after 1 month of life, and were compared to those of control infants (birth weight = 3400 +/- 198 g at term) of healthy mothers. Compared to controls, at birth, macrosomic newborns had higher serum lipids, apolipoprotein A-I and B-100, and lipoprotein (very low density lipo…

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein BBirth weightLipoproteinsPregnancy in DiabeticsBlood lipidsFetal Macrosomiachemistry.chemical_compoundPregnancyReference ValuesInternal medicineDiabetes mellitusmedicineHumanschemistry.chemical_classificationbiologybusiness.industryFatty AcidsInfant NewbornFatty acidmedicine.diseaseLipidsEndocrinologyDiabetes Mellitus Type 1chemistryLow-density lipoproteinCase-Control StudiesPediatrics Perinatology and Child Healthbiology.proteinlipids (amino acids peptides and proteins)FemalebusinessLipoproteinEuropean journal of pediatrics
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A targeted apoB38.9 mutation in mice is associated with reduced hepatic cholesterol synthesis and enhanced lipid peroxidation.

2006

Familial hypobetalipoproteinemia (FHBL) due to truncation-specifying mutations of apolipoprotein B (apoB), which impair hepatic lipid export in very low-density lipoprotein (VLDL) particles, is associated with fatty liver. In an FHBL-like mouse with the apoB38.9 mutation, fatty liver develops despite reduced hepatic fatty acid synthesis. However, hepatic cholesterol contents in apoB38.9 mice are normal. We found that cholesterogenic enzymes (3-hydroxy-3-methylglutaryl-coenzyme A reductase, sterol-C5-desaturase, and 7-dehydrocholesterol reductase) were consistently downregulated in two separate expression-profiling experiments using a total of 19 mice ( n = 7 each for apob+/+and apob+/38.9, …

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein BPhysiologymedicine.disease_causeLipid peroxidationHypobetalipoproteinemiaschemistry.chemical_compoundMicePhysiology (medical)Internal medicineNAFLDmedicineAnimalsFamilial hypobetalipoproteinemiamice modelCells CulturedApolipoproteins BMutationHepatologybiologyChemistryMutagenesisGastroenterologyGene targetingRatsFatty LiverMice Inbred C57BLEndocrinologyCholesterolLiverApolipoprotein B-100Gene Targetingbiology.proteinHepatocytesMutagenesis Site-Directedlipids (amino acids peptides and proteins)Lipid PeroxidationmutationOxidative stressLipoproteinAmerican journal of physiology. Gastrointestinal and liver physiology
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Platelet sensitivity to prostacyclin and thromboxane production in hyperlipidemic patients

1982

SummaryIn 13 type II hyperlipidemics (10 males and 3 females; mean age 50.2 ± 10.6 years), in 10 type IV hyperlipidemics (7 males and 3 females; mean age 51 ± 13.3 years) and in 23 healthy age-and sex-matched controls, the following parameters were measured: plasma cholesterol; plasma TG; plasma C-HDL; VLDL, separated in a preparative ultracentrifuge; C-LDL; Apo B, with immunoelectrophoretic method; platelet sensitivity to prostacyclin; TXB2 formation in PRP; TXB2 in serum.This study provides evidence for: 1. Reduced platelet sensitivity to prostacyclin, more evident in type II hyperlipidemia that provides an additional mechanism involved in increased platelet aggregation found in type II h…

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein BbiologyChemistryProstacyclinStimulationHematologyThromboxane ProductionEndocrinologyThrombinInternal medicinemedicinebiology.proteinlipids (amino acids peptides and proteins)PlateletThromboxane-A synthasemedicine.drug
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Polymorphisms at theSRBIlocus are associated with lipoprotein levels in subjects with heterozygous familial hypercholesterolemia

2002

Scavenger receptor, class B, type 1 (SRBI) is a promising candidate gene involved in the pathophysiology of atherosclerosis. We have examined the association of three common polymorphisms at the SRBI locus in 77 subjects who were heterozygous for familial hypercholesterolemia (FH). The alleles represented by polymorphisms in exon 1 and exon 8 were associated with variation in plasma concentrations of fasting triglyceride (TG). Mean plasma TG concentrations for homozygotes for the most common allele, and for heterozygotes and homozygotes for the less common allele were 85 +/- 6, 111 +/- 9 and 135 +/- 22 mg/dl (p = 0.011) for exon 1, and 96 +/- 11, 86 +/- 6 and 134 +/- 13 mg/dl (p = 0.007) fo…

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein BbiologyTriglycerideCholesterolFamilial hypercholesterolemiamedicine.diseasechemistry.chemical_compoundEndocrinologychemistryLow-density lipoproteinInternal medicineGeneticsbiology.proteinmedicinelipids (amino acids peptides and proteins)Scavenger receptorGenetics (clinical)LipoproteinClinical Genetics
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In vivo metabolism of LDL subfractions in patients with heterozygous FH on statin therapy

2004

LDL can be subfractionated into buoyant (1.020-1.029 g/ml(-1)), intermediate (1.030-1.040 g/ml(-1)), and dense (1.041-1.066 g/ml(-1)) LDLs. We studied the rebound of these LDL-subfractions after LDL apheresis in seven patients with heterozygous familial hypercholesterolemia (FH) regularly treated by apheresis (58 +/- 9 years, LDL-cholesterol = 342 +/- 87 mg/dl(-1), triglycerides = 109 +/- 39 mg/dl(-1)) and high-dose statins. Apolipoprotein B (apoB) concentrations were measured in LDL subfractions immediately after and on days 1, 2, 3, 5, and 7 after apheresis. Compartmental models were developed to test three hypotheses: 1) that dense LDLs are derived from the delipidation of buoyant and in…

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein Blow density lipoprotein metabolismFamilial hypercholesterolemiaQD415-436Biochemistrychemistry.chemical_compoundEndocrinologyInternal medicinerebound kineticsmedicinesmall dense low density lipoproteinsdensity gradient ultracentrifugationbiologyfamilial hypercholesterolemiaChemistryCholesterollow density lipoprotein subtypesCell BiologyMetabolismmedicine.diseaseEndocrinologyApheresisLDL apheresisbiology.proteinDensity gradient ultracentrifugationlipids (amino acids peptides and proteins)Journal of Lipid Research
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Dietary cholate increases plasma levels of apolipoprotein B in mice by posttranscriptional mechanisms

2001

To induce atherogenesis in mice, a high fat (HF) diet is supplemented with cholic acid (CA), which increases apoB-containing particles and lower apoA-I-containing particles. HF diet without CA increases levels of both HDL and LDL, suggesting that CA may be responsible for the elevation of LDL and lowering of HDL. The mechanism of dietary CA-induced lowering of apoA-I-containing particles has recently been reported. In this study, we examined the mechanism of CA- and HF-induced elevation of apoB-containing lipoproteins in mice. Mice were fed the following four diets: control chow (C), high fat high cholesterol, (HF), control and 0.5% cholate (CA), and HF + CA. Dietary CA increased the plasma…

medicine.medical_specialtyVery low-density lipoproteinSettore MED/09 - Medicina InternaMouseApolipoprotein Bmedicine.medical_treatmentDown-RegulationCholic AcidLipoproteins VLDLBiochemistryDietary cholateMicechemistry.chemical_compoundApolipoproteins ERibonucleasesDownregulation and upregulationInternal medicinemedicineAnimalsVitamin ERNA MessengerRNA Processing Post-TranscriptionalReceptorApolipoproteins BbiologyChemistryVitamin ECholic acidnutritional and metabolic diseasesCell BiologyBlotting NorthernDietLipoproteins LDLMice Inbred C57BLCholesterolEndocrinologyLiverReceptors LDLLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Gene expressionHepatic lipaseApolipoprotein BCholatesDietary fatThe International Journal of Biochemistry & Cell Biology
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Establishing cut-off values for apolipoprotein B and non-HDL-C according to LDL-C values in a South European population

2012

SUMMARY Background: Low-density lipoprotein cholesterol (LDL-C) remains the primary target of therapy in most strategies of dyslipidaemia management focused on cardiovascular disease prevention. Different guidelines have identified specific LDL-C cut-off points as targets for therapeutic intervention. Many clinical situations characterised by dyslipidaemia and elevated triglycerides are common in our environment and in overall industrialised countries. Thus, lipid goals based only on LDL-C could misclassify an important percentage of subjects. The objective of the present study was to establish cut-off point values for apoB and non-HDL-C in relation to the identified LDL-C cut-off points fo…

medicine.medical_specialtyeducation.field_of_studyApolipoprotein BbiologyCross-sectional studybusiness.industryCholesterolNon hdl cPopulationnutritional and metabolic diseasesGeneral MedicineEuropean populationchemistry.chemical_compoundEndocrinologychemistryInternal medicinemedicinebiology.proteinlipids (amino acids peptides and proteins)Young adultbusinesseducationLipoprotein cholesterolInternational Journal of Clinical Practice
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Oxidative Stress and Antioxidant Levels in Patients with Anorexia Nervosa after Oral Re-alimentation: A Systematic Review and Exploratory Meta-analys…

2015

Oxidative stress markers seem to be higher in patients with anorexia nervosa (AN) than healthy controls, but the potentially beneficial effects of weight gain is not known. We calculated random effects standardised mean differences (SMDs) as effect size measures of oxidative stress marker changes after re-alimentation reported in two or more studies, summarising others descriptively. Seven longitudinal studies (n = 104) were included. After a median follow-up period of 8 weeks, AN patients significantly increased their body mass index (15.1 ± 2.1 to 17.1 ± 2.2, p < 0.0001). This weight gain was followed by a significant increase in serum levels of the antioxidant albumin (studies = 6, SM…

oxidative streantioxidantSuperoxide DismutaseMedicine (all)weight gainCatalaseAntioxidantsanorexia nervosaOxidative StressClinical PsychologyPsychiatry and Mental HealthAlbuminsApolipoprotein B-100albumin; anorexia nervosa; antioxidant; ApoB; oxidative stress; refeeding; weight gain; Albumins; Anorexia Nervosa; Antioxidants; Apolipoprotein B-100; Biomarkers; Catalase; Humans; Longitudinal Studies; Superoxide Dismutase; Weight Gain; Oxidative Stress; Clinical Psychology; Psychiatry and Mental Health; Medicine (all)HumansLongitudinal StudiesApoBApoB; albumin; anorexia nervosa; antioxidant; oxidative stress; refeeding; weight gainBiomarkersalbuminrefeeding
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Induction of body weight loss through RNAi-knockdown of APOBEC1 gene expression in transgenic rabbits

2014

In the search of new strategies to fight against obesity, we targeted a gene pathway involved in energy uptake. We have thus investigated the APOB mRNA editing protein (APOBEC1) gene pathway that is involved in fat absorption in the intestine. The APOB gene encodes two proteins, APOB100 and APOB48, via the editing of a single nucleotide in the APOB mRNA by the APOBEC1 enzyme. The APOB48 protein is mandatory for the synthesis of chylomicrons by intestinal cells to transport dietary lipids and cholesterol. We produced transgenic rabbits expressing permanently and ubiquitously a small hairpin RNA targeting the rabbit APOBEC1 mRNA. These rabbits exhibited a moderately but significantly reduced …

perte de poidsobesityApolipoprotein BAgricultural BiotechnologyGene Expressionlcsh:MedicinetransgenesisSmall hairpin RNAAnimals Genetically Modified0302 clinical medicinesirnaRNA interferenceGene expressionGene Knockdown TechniquesBiologie de la reproductionMedicine and Health SciencesTransgenesIntestinal MucosaRNA Small Interferinglcsh:Science[SDV.BDD]Life Sciences [q-bio]/Development Biology2. Zero hunger0303 health sciencesGene knockdownReproductive BiologyMultidisciplinarybiologyGenetically Modified OrganismsBiologie du développementapobec1; obesity; editing apob; apob100; apob48; chylomicron; intestine; rabbit; sirna; transgenesis; knockdownchylomicronknockdownAgricultureInherited Metabolic DisordersDevelopment BiologyobésitéCholesterolPhenotypeTransgenic Engineering[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive BiologyLiverapobapob48Gene Knockdown Techniquesanimal transgéniqueRNA Interferencelipids (amino acids peptides and proteins)RabbitsGenetic EngineeringResearch ArticleBiotechnologyexpression géniqueTransgeneAPOBEC-1 DeaminaseMolecular Sequence DatarabbitDiet High-Fat03 medical and health sciencesintestinCytidine DeaminaseWeight Loss[SDV.BDD] Life Sciences [q-bio]/Development BiologyAnimalsHumanslapinRNA Messenger[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyintestineTriglycerides[SDV.BDLR] Life Sciences [q-bio]/Reproductive Biology030304 developmental biologyapobec1Base SequenceGenetically Modified AnimalsAPOBEC1editinglcsh:RBiology and Life Sciences[SDV.BDLR]Life Sciences [q-bio]/Reproductive BiologyMolecular biologyapob100DyslipidemiaMetabolic Disordersbiology.proteinlcsh:QRNA EditingApolipoprotein B-48030217 neurology & neurosurgery
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