Search results for " LOW-DENSITY LIPOPROTEIN"

showing 10 items of 96 documents

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Estimation of serum lipids in patients with Oral Submucous Fibrosis in India

2014

Objectives: Oral submucous fibrosis (OSMF) is the most prevalent precancerous condition in India. Low levels of lipids serves as a marker and prognostic indicator in the early detection of oral precancerous and cancerous states. In spite of the high prevalence and its potential to undergo malignant transformation, this condition has not widely been investigated with respect to the serum lipid levels. In the present study, an attempt was made to analyze the complete serum lipid profile, total cholesterol (TC), triglycerides (TG), high density lipoprotein (HDL) choleste - rol, low density lipoprotein (LDL) cholesterol and very low density lipoprotein (VLDL) cholesterol in OSMF and controls. M…

medicine.medical_specialtyVery low-density lipoproteinBlood lipidsOdontologíaGastroenterologychemistry.chemical_compoundHigh-density lipoproteinInternal medicinemedicineGeneral DentistryOral Medicine and Pathologymedicine.diagnostic_testCholesterolbusiness.industryResearchmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludPrecancerous conditionEndocrinologychemistryOral submucous fibrosisLow-density lipoproteinUNESCO::CIENCIAS MÉDICASlipids (amino acids peptides and proteins)businessLipid profile
researchProduct

La auténtica dimensión del colesterol-no-HDL: colesterol aterogénico

2016

Lowe density lipoproteins (LDL) are the causal agent of cardiovascular diseases. In practice, we identify LDL with cholesterol transported in LDL (cLDL). So, cLDL has become the major target for cardiovascular prevention. Howewer, we have progressive evidences about the role of triglycerides rich lipoproteins, particularly those very low density lipoprotein (VLDL) in promotion and progression of atherosclerosis, that leads cholesterol in VLDL and its remanents as a potential therapeutic target. This feature is particularly important and of a great magnitude, in patients with hypertiglyceridemia. We can to considere, that the non-HDL cholesterol -cLDL+cVLDL+c-remmants+Lp(a)- is the real meas…

medicine.medical_specialtyVery low-density lipoproteinHigh risk patientsbusiness.industryCholesterolHypertriglyceridemia030204 cardiovascular system & hematologymedicine.disease03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePostprandialEndocrinologyCardiovascular preventionchemistryInternal medicineNon hdl cholesterolmedicinelipids (amino acids peptides and proteins)Pharmacology (medical)In patient030212 general & internal medicineCardiology and Cardiovascular MedicinebusinessClínica e Investigación en Arteriosclerosis
researchProduct

Statins and diabetes.

2005

Lipid abnormalities play an important part in raising the cardiovascular risk in diabetic subjects. The main components of diabetic dyslipidemia are increased plasma triglycerides, low concentration of high-density lipoprotein cholesterol, preponderance of small, dense low-density lipoprotein, and excessive postprandial lipemia. Small, dense low-density lipoprotein, the elevation in remnant triglyceride-rich lipoprotein particles, and the low high-density lipoprotein are the most powerful atherogenic components. The coexistence of these three factors strongly aggravates the lipid accumulation in the arterial wall and the formation of atherosclerotic plaques. The position of diabetes in card…

medicine.medical_specialtyVery low-density lipoproteinHyperlipidemiasType 2 diabeteschemistry.chemical_compoundInsulin resistanceRisk FactorsInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansTriglyceridebusiness.industrymedicine.diseaseLipidsEndocrinologychemistryCardiovascular Diseaseslipids (amino acids peptides and proteins)Therapeutic Lifestyle ChangesMetabolic syndromeHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessLipoproteinSeminars in vascular medicine
researchProduct

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
researchProduct

Statins and metabolic syndrome

2003

Abstract Metabolic syndrome (MS) is a multifactorial condition that represents a risk factor for the development of diabetes mellitus (DMII) and cardiovascular disease (CVD). Statins may play a role on some modifiable clinical features of MS; in fact, whereas therapeutic lifestyle changes are mandatory for MS with a 10-year coronary heart disease (CHD) risk 20% and to correct the other associated lipid and non-lipid abnormalities. In fact, they have a VLDL lowering action in hypertriglyceridemia, they reduce the amount of small and dense LDL, they increase the HDL-C, they reduce the atherogenic lipoproteins, and they decrease the inflammatory marker levels.

medicine.medical_specialtyVery low-density lipoproteinbusiness.industryHypertriglyceridemianutritional and metabolic diseasesGeneral MedicineDiseasemedicine.diseaseEndocrinologyDiabetes mellitusInternal medicinemedicineCardiologylipids (amino acids peptides and proteins)RosuvastatinTherapeutic Lifestyle ChangesMetabolic syndromeRisk factorbusinessmedicine.drugInternational Congress Series
researchProduct