Search results for "QD415"

showing 10 items of 87 documents

Differential effects of the C1431T and Pro12Ala PPARgamma gene variants on plasma lipids and diabetes risk in an Asian population.

2004

We investigated the association of C1431T and Pro12Ala polymorphisms at the peroxisome proliferator-activated receptor γ (PPARγ) locus with plasma lipids and insulin resistance-related variables, according to diabetes status, in a large and representative Asian population from Singapore consisting of 2,730 Chinese, 740 Malays, and 568 Indians. Moreover, we estimated the diabetes risk and examined gene-nutrient interactions between these variants and the ratio of polyunsaturated fatty acid to saturated fat (SFA) in determining body mass index (BMI) and fasting insulin. We found differential effects of these gene variants. The Pro12Ala polymorphism was more associated with plasma lipids and f…

AdultBlood GlucoseMalemedicine.medical_specialtyDiabetes riskAsiaSaturated fatmedicine.medical_treatmentMutation MissensePeroxisome proliferator-activated receptorLocus (genetics)QD415-436BiologyBiochemistryPolymorphism Single NucleotidepolymorphismBody Mass IndexEndocrinologyRisk FactorsfatDiabetes mellitusInternal medicinemedicineDiabetes MellitusHumansInsulinAllelechemistry.chemical_classificationperoxisome proliferator-activated receptorInsulinFatty AcidsCell BiologyMiddle Agedmedicine.diseaseLipidsPPAR gammaEndocrinologychemistryFatty Acids UnsaturatedFemaleInsulin ResistancedietBody mass indexJournal of lipid research
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Associations of LPL and APOC3 gene polymorphisms on plasma lipids in a mediterranean population: Interaction with tobacco smoking and the APOE locus

2002

We conducted a cross-sectional study in a Spanish population (n = 1,029) to investigate associations between the LPL and APOC3 gene loci (LPL-HindIII, LPL-S447X, and APOC3-SstI) and plasma lipid levels and their interaction with APOE polymorphisms and smoking. Carriers of the H− or the X447 allele had higher levels of HDL cholesterol (HDL-C), and lower levels of TG, after adjustment for age, body mass index, alcohol, smoking, exercise, and education (P < 0.01). The APOC3 polymorphism presented additive effects to the LPL variants on TG and HDL-C levels in men, and on TG in women. The most and the least favorable haplotype combinations were H−/X447/S1 and H+/S447/S2, respectively. These comb…

AdultMaleApolipoprotein Emedicine.medical_specialtyapolipoprotein C-IIIPopulationlipoprotein lipaseLocus (genetics)Deoxyribonuclease HindIIIQD415-436Biochemistrylipidschemistry.chemical_compoundApolipoproteins EEndocrinologyInternal medicineHumansMedicineAlleleApolipoproteins CDeoxyribonucleases Type II Site-SpecificeducationTriglyceridesGeneticseducation.field_of_studyLipoprotein lipasePolymorphism Geneticbusiness.industryCholesterolCholesterol HDLSmokingHaplotypeGenetic Variationnutritional and metabolic diseasesCell BiologyCross-Sectional StudiesEndocrinologychemistrySpainFemalelipids (amino acids peptides and proteins)gene-environmental interactionbusinessBody mass index
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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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Phytosterol plasma concentrations and coronary heart disease in the prospective Spanish EPIC cohort

2010

Phytosterol intake with natural foods, a measure of healthy dietary choices, increases plasma levels, but increased plasma phytosterols are believed to be a coronary heart disease (CHD) risk factor. To address this paradox, we evaluated baseline risk factors, phytosterol intake, and plasma noncholesterol sterol levels in participants of a case control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) Spanish cohort who developed CHD (n = 299) and matched controls (n = 584) who remained free of CHD after a 10 year follow-up. Sitosterol-to-cholesterol ratios increased across tertiles of phytosterol intake (P = 0.026). HDL-cholesterol level increased, …

AdultMalecampesterolmedicine.medical_specialtyCampesterolPopulationCoronary DiseaseLathosterolQD415-436lathosterolBiochemistryplant sterolsCohort Studieschemistry.chemical_compoundEndocrinologyRisk FactorsInternal medicineHumansMedicineProspective StudiesRisk factoreducationProspective cohort studyAgededucation.field_of_studyCholesterolbusiness.industrycholesterolPhytosterolsCell BiologyEuropean Prospective Investigation into Cancer and NutritionMiddle AgedDietEuropean Prospective Investigation into Cancer and NutritionEndocrinologysitosterolchemistrySpainCase-Control StudiesNested case-control studyFemalelipids (amino acids peptides and proteins)Patient-Oriented and Epidemiological ResearchbusinessJournal of Lipid Research
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Inability of HDL from abdominally obese subjects to counteract the inhibitory effect of oxidized LDL on vasorelaxation.

2007

Abdominal obesity is associated with a decreased plasma concentration of HDL cholesterol and with qualitative modifications of HDL, such as triglyceride enrichment. Our aim was to determine, in isolated aorta rings, whether HDL from obese subjects can counteract the inhibitory effect of oxidized low density lipoprotein (OxLDL) on endothelium-dependent vasodilation as efficiently as HDL from normolipidemic, lean subjects. Plasma triglycerides were 74% higher (P < 0.005) in obese subjects compared with controls, and apolipoprotein A-I (apoA-I) and HDL cholesterol concentrations were 12% and 17% lower (P < 0.05), respectively. HDL from control subjects significantly reduced the inhibitory effe…

AdultMalemedicine.medical_specialtyApolipoprotein BVasodilator Agentsapolipoprotein A-IVasodilationQD415-436In Vitro TechniquesBiochemistrychemistry.chemical_compoundEndocrinologyHigh-density lipoproteinInternal medicinemedicineAnimalsHumansObesityInhibitory effectAbdominal obesityAortaTriglyceridesbiologyTriglycerideCholesterolCholesterol HDLnutritional and metabolic diseasesCell BiologyMiddle Agedmedicine.diseaseObesityAcetylcholineLipoproteins LDLVasodilationEndocrinologychemistryhigh density lipoproteinbiology.proteinoxidized low density lipoproteinlipids (amino acids peptides and proteins)FemaleCholesterol EstersRabbitsmedicine.symptomJournal of lipid research
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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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Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
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Hsp70 and Its Molecular Role in Nervous System Diseases

2011

Heat shock proteins (HSPs) are induced in response to many injuries including stroke, neurodegenerative disease, epilepsy, and trauma. The overexpression of one HSP in particular, Hsp70, serves a protective role in several different models of nervous system injury, but has also been linked to a deleterious role in some diseases. Hsp70 functions as a chaperone and protects neurons from protein aggregation and toxicity (Parkinson disease, Alzheimer disease, polyglutamine diseases, and amyotrophic lateral sclerosis), protects cells from apoptosis (Parkinson disease), is a stress marker (temporal lobe epilepsy), protects cells from inflammation (cerebral ischemic injury), has an adjuvant role i…

Autoimmune diseasebusiness.industryMultiple sclerosisNeurodegenerationReview ArticleDiseaseHsp70 nervous system neurodegenerative diseasesmedicine.diseaseBiochemistrylcsh:BiochemistryCellular stress responseHeat shock proteinImmunologymedicinelcsh:QD415-436Alzheimer's diseaseAmyotrophic lateral sclerosisbusinessBiochemistry Research International
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Obesity alters the gustatory perception of lipids in the mouse: plausible involvement of lingual CD36. : Obesity decreases the fat preference

2013

International audience; A relationship between orosensory detection of dietary lipids, regulation of fat intake, and body mass index was recently suggested. However, involved mechanisms are poorly understood. Moreover, whether obesity can directly modulate preference for fatty foods remains unknown. To address this question, exploration of the oral lipid sensing system was undertaken in diet-induced obese (DIO) mice. By using a combination of biochemical, physiological, and behavioral approaches, we found that i) the attraction for lipids is decreased in obese mice, ii) this behavioral change has an orosensory origin, iii) it is reversed in calorie-restricted DIO mice, revealing an inverse …

CD36 AntigensCD36[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionAdipose tissueMESH : Behavior AnimalBiochemistryCalcium in biologyMice0302 clinical medicineEndocrinologyMESH : Calcium SignalingMESH: Behavior AnimalMESH: ObesityMESH: AnimalsLingual papillaResearch Articles2. Zero hunger0303 health sciencesMESH : Food PreferencesBehavior AnimalMESH : TongueMESH : Diet High-FatMESH: TongueTaste Perceptiontaste sensitivityMESH : Antigens CD36calcium imagingAdipose TissueHealthMESH: Dietary FatsMESH : ObesityFat tasteMESH: Adipose Tissuemedicine.medical_specialtyFood behavior030209 endocrinology & metabolismMESH : Mice Inbred C57BLQD415-436BiologyDiet High-FatMESH: Calcium SignalingMESH : Adipose TissueFood Preferences03 medical and health sciencesCalcium imagingTongueDownregulation and upregulationMESH: Mice Inbred C57BLInternal medicineMESH : MicemedicineAnimalsCalcium SignalingObesityFatty acidsMESH: Food PreferencesMESH: Mice030304 developmental biologyNutritionlong-chain fatty acidsMESH: Antigens CD36MESH : Taste PerceptionCell Biologymedicine.diseaseDietary FatsObesityMice Inbred C57BLMESH: Diet High-FatEndocrinologyMESH: Taste Perceptionbiology.proteinMESH : AnimalsBody mass index[SDV.AEN]Life Sciences [q-bio]/Food and NutritionMESH : Dietary Fats
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Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity

2012

Glucagon-like peptide-1 (GLP-1) signaling modulates sweet-taste sensitivity in the mouse. Because circumvallate papillae (CVPs) express both GLP-1 and its receptor, a local regulation has been suggested. However, whether dietary lipids are involved in this regulation, as shown in the gut, is unknown. By using a combination of biochemical, immunohistochemical, and behavioral approaches, the present data i) confirm the role of GLP-1 signaling in the attraction for sucrose, ii) demonstrate that minute quantities of long-chain FAs (LCFAs) reinforce the attraction for sucrose in a GLP-1 receptor-dependent manner, iii) suggest an involvement of the LCFA receptor GPR120 expressed in taste buds in …

CD36 Antigensmedicine.medical_specialtyTasteendocrine systemCD36Blotting WesternQD415-436eating behaviorReal-Time Polymerase Chain ReactionBiochemistryGlucagon-Like Peptide-1 ReceptorReceptors G-Protein-CoupledMiceEndocrinologyTAS1R3TAS1R2Glucagon-Like Peptide 1Cell Line TumorInternal medicinelong-chain fatty acidReceptors GlucagonmedicineAnimalsHumansSecretionObesityReceptorLingual papillaResearch Articlesbiologydigestive oral and skin physiologyGPR120healthCell BiologyTaste BudsImmunohistochemistryMice Inbred C57BLEndocrinologyobesity riskbiology.proteinJournal of Lipid Research
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