Search results for " Metabolic diseases"

showing 10 items of 699 documents

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
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Plasma metabolites predict both insulin resistance and incident type 2 diabetes: a metabolomics approach within the Prevención con Dieta Mediterránea…

2019

Background Insulin resistance is a complex metabolic disorder and is often associated with type 2 diabetes (T2D). Objectives The aim of this study was to test whether baseline metabolites can additionally improve the prediction of insulin resistance beyond classical risk factors. Furthermore, we examined whether a multimetabolite model predicting insulin resistance in nondiabetics can also predict incident T2D. Methods We used a case-cohort study nested within the Prevencion con Dieta Mediterranea (PREDIMED) trial in subsets of 700, 500, and 256 participants without T2D at baseline and 1 and 3 y. Fasting plasma metabolites were semiquantitatively profiled with liquid chromatography-tandem m…

0301 basic medicineMalemedicine.medical_specialtyendocrine system diseasesMetaboliteMedicine (miscellaneous)030209 endocrinology & metabolismType 2 diabetesDiet MediterraneanGastroenterologyCohort Studies03 medical and health scienceschemistry.chemical_compoundPlasma0302 clinical medicineMetabolomicsInsulin resistanceRisk FactorsInternal medicinemedicineHumansInsulinMetabolomicsAgedProportional Hazards ModelsNutrition and Dieteticsbusiness.industryIncidence (epidemiology)Metabolic disorderArea under the curvenutritional and metabolic diseasesRegression analysisFastingMiddle Agedmedicine.diseaseOriginal Research Communications030104 developmental biologychemistryDiabetes Mellitus Type 2FemaleInsulin Resistancebusiness
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Decrease in αβ/γδ T-cell ratio is accompanied by a reduction in high-fat diet-induced weight gain, insulin resistance, and inflammation.

2018

The implication of αβ and γδ T cells in obesity-associated inflammation and insulin resistance (IR) remains uncertain. Mice lacking γδ T cells show either no difference or a decrease in high-fat diet (HFD)-induced IR, whereas partial depletion in γδ T cells does not protect from HFD-induced IR. αβ T-cell deficiency leads to a decrease in white adipose tissue (WAT) inflammation and IR without weight change, but partial depletion of these cells has not been studied. We previously described a mouse model overexpressing peroxisome proliferator-activated receptor β (PPAR-β) specifically in T cells [transgenic (Tg) T-PPAR-β] that exhibits a partial depletion in αβ T cells and no change in γδ T-ce…

0301 basic medicineMalemedicine.medical_specialtymedicine.medical_treatmentT cellReceptors Antigen T-Cell alpha-betaT-LymphocytesAdipose tissueInflammationWhite adipose tissueDiet High-FatWeight GainBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemInsulin resistanceInternal medicineGlucose IntoleranceGeneticsmedicineAnimalsObesityMolecular BiologyInflammationChemistryInsulinWeight changeBody Weightfood and beveragesnutritional and metabolic diseasesReceptors Antigen T-Cell gamma-deltamedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologymedicine.anatomical_structurelipids (amino acids peptides and proteins)medicine.symptomInsulin Resistancehormones hormone substitutes and hormone antagonists030217 neurology & neurosurgeryBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Gut Microbiome Associates With Lipid-Lowering Effect of Rosuvastatin in Vivo

2018

Source at https://doi.org/10.3389/fmicb.2018.00530 . Background: Statin has been widely used to treat hyperlipidemia because of its high potency in decreasing cholesterol levels. The present study aimed to examine the lipid-lowering effect of rosuvastatin and the composition, diversity and species abundance of gut microbiome in association with rosuvastatin efficacy. TRIAL REGISTRATION: ChiCTR-ORC-17013212 at the First Affiliated Hospital of Dalian Medical University, November 2, 2017. Results:Totally 64 patients with hyperlipidemia were treated with 10 mg/day of rosuvastatin for 4-8 weeks. Blood lipid indicators triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL), lo…

0301 basic medicineMicrobiology (medical)Statinmedicine.drug_classlcsh:QR1-502PhysiologyBlood lipidsgut microbiomeBiologyGut floraMicrobiologylcsh:Microbiology03 medical and health scienceschemistry.chemical_compoundHigh-density lipoproteinHyperlipidemiamedicinehyperlipidemiaRosuvastatinVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Cardiology: 771VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Kardiologi: 771CholesterolVDP::Medical disciplines: 700::Basic medical dental and veterinary science disciplines: 710::Pharmacology: 728nutritional and metabolic diseasesFusobacteriaVDP::Medical disciplines: 700::Basic medical dental and veterinary science disciplines: 710::Medical microbiology: 715medicine.diseasebiology.organism_classification16S rRNA sequencing030104 developmental biologychemistryVDP::Medisinske Fag: 700::Basale medisinske odontologiske og veterinærmedisinske fag: 710::Medisinsk mikrobiologi: 715VDP::Medisinske Fag: 700::Basale medisinske odontologiske og veterinærmedisinske fag: 710::Farmakologi: 728lipids (amino acids peptides and proteins)hypolipidemic effectrosuvastatinmedicine.drugFrontiers in Microbiology
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The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated fr…

2016

It is not known if the mitochondria-targeted antioxidants such as mitoquinone (MitoQ) can modulate oxidative stress and leukocyte-endothelium interactions in T2D patients. We aimed to evaluate the beneficial effect of MitoQ on oxidative stress parameters and leukocyte-endothelium interactions in leukocytes of T2D patients. The study population consisted of 98 T2D patients and 71 control subjects. We assessed metabolic and anthropometric parameters, mitochondrial reactive oxygen species (ROS) production, glutathione peroxidase 1 (GPX-1), NFκB-p65, TNFα and leukocyte-endothelium interactions. Diabetic patients exhibited higher weight, BMI, waist circumference, SBP, DBP, glucose, insulin, HOMA…

0301 basic medicineMitochondrial ROSMaleGPX1Antioxidantendocrine system diseasesUbiquinonemedicine.medical_treatmentBMI body mass indexClinical BiochemistryLDL low density lipoprotein cholesterolAnti-Inflammatory AgentsTPP triphenylphosphonium030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeBiochemistryMitoQAntioxidantschemistry.chemical_compound0302 clinical medicineGlutathione Peroxidase GPX1IR insulin resistanceLeukocyteslcsh:QH301-705.5chemistry.chemical_classificationlcsh:R5-920AnthropometryChemistryGlutathione peroxidaseType 2 diabetesMiddle AgedFemalemedicine.symptomlcsh:Medicine (General)Research PaperPMN polymorphonuclear leukocyteshs-CRP high-sensitive C-reactive proteinHOMA-IR homeostasis model assessment of insulin resistanceInflammationT2D type 2 diabetes03 medical and health sciencesOrganophosphorus CompoundsmedicineDBP diastolic blood pressure HbA1c glycated hemoglobinHUVEC human umbilical vein endothelial cellsHumansEndotheliumAgedInflammationReactive oxygen speciesMitoQGlutathione PeroxidaseTumor Necrosis Factor-alphaSBP systolic blood pressureOrganic ChemistryTranscription Factor RelAnutritional and metabolic diseasesHDL high density lipoprotein cholesterolOxidative Stress030104 developmental biologylcsh:Biology (General)Diabetes Mellitus Type 2ImmunologyReactive Oxygen SpeciesOxidative stressRedox Biology
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Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?

2017

Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert t…

0301 basic medicineMitochondrial ROSMaleGPX1endocrine system diseasesPhysiologyClinical Biochemistry030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry0302 clinical medicineSuperoxide Dismutase-1Glutathione Peroxidase GPX1Sirtuin 3LeukocytesGeneral Environmental Sciencechemistry.chemical_classificationbiologyMiddle AgedCatalaseIntercellular Adhesion Molecule-1MetforminMetforminP-SelectinCatalaseFemalemedicine.drugmedicine.medical_specialtySIRT3Superoxide dismutase03 medical and health sciencesInternal medicinemedicineCell AdhesionHumansHypoglycemic AgentsMolecular BiologyAgedReactive oxygen speciesGlutathione Peroxidasenutritional and metabolic diseasesEndothelial CellsCell BiologyOxidative Stress030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2biology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidantsredox signaling
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Insulin Resistance in PCOS Patients Enhances Oxidative Stress and Leukocyte Adhesion: Role of Myeloperoxidase

2016

Cardiovascular diseases and oxidative stress are related to polycystic ovary syndrome (PCOS) and insulin resistance (IR). We have evaluated the relationship between myeloperoxidase (MPO) and leukocyte activation in PCOS patients according to homeostatic model assessment of IR (HOMA-IR), and have explored a possible correlation between these factors and endocrine and inflammatory parameters. This was a prospective controlled study conducted in an academic medical center. The study population consisted of 101 PCOS subjects and 105 control subjects. We divided PCOS subjects into PCOS non-IR (HOMA-IR2.5). Metabolic and anthropometric parameters, total and mitochondrial reactive oxygen species (…

0301 basic medicineMitochondrial ROSendocrine system diseasesmedicine.medical_treatment030204 cardiovascular system & hematologyPathology and Laboratory Medicinemedicine.disease_causeBiochemistryWhite Blood CellsFluorescence MicroscopyEndocrinology0302 clinical medicineAnimal CellsMedicine and Health SciencesLeukocytesInsulinImmune ResponseEnergy-Producing OrganellesMicroscopyMultidisciplinaryQRLight MicroscopyPolycystic ovaryMitochondriaOncologyMyeloperoxidaseHomeostatic model assessmentCytokinesMedicineFemaleCellular TypesCellular Structures and OrganellesInflammation MediatorsResearch ArticlePolycystic Ovary SyndromeAdultmedicine.medical_specialtyAdhesion MoleculesImmune CellsScienceImmunologyBioenergeticsBiologyResearch and Analysis MethodsProinflammatory cytokineYoung Adult03 medical and health sciencesSigns and SymptomsInsulin resistanceDiagnostic MedicineInternal medicineCell AdhesionmedicineHumansPeroxidaseInflammationDiabetic EndocrinologyBlood CellsInsulinBiology and Life SciencesCancers and Neoplasmsnutritional and metabolic diseasesCell BiologyMolecular Developmentmedicine.diseaseHormonesOxidative Stress030104 developmental biologyEndocrinologybiology.proteinInsulin ResistanceReactive Oxygen SpeciesGynecological TumorsOxidative stressDevelopmental Biology
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Associations of Pathogenic Variants in MLH1, MSH2, and MSH6 With Risk of Colorectal Adenomas and Tumors and With Somatic Mutations in Patients With L…

2020

Contains fulltext : 220040.pdf (Publisher’s version ) (Closed access) BACKGROUND & AIMS: Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an increased risk of colorectal cancer (CRC). In patients with Lynch syndrome, CRCs can develop via different pathways. We studied associations between Lynch syndrome-associated variants in MMR genes and risks of adenoma and CRC and somatic mutations in APC and CTNNB1 in tumors in an international cohort of patients. METHODS: We combined clinical and molecular data from 3 studies. We obtained clinical data from 2747 patients with Lynch syndrome associated with variants in MLH1, MSH2, or MSH6 from Germany, the Net…

0301 basic medicineOncologyMaleColorectal cancerDNA Mutational Analysisgenetic analysisHEREDITARYcancer riskGUIDELINESDNA Mismatch Repair0302 clinical medicineGermanyTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Prospective Studiesprognostic factorFinlandbeta CateninNetherlandsOutcomePrognostic FactorGastroenterologyGenetic AnalysisColonoscopyMiddle AgedCANCERLynch syndromeCancer Risk3. Good healthDNA-Binding ProteinsDEFICIENCYMutS Homolog 2 Proteinsyöpägeenitoutcome030211 gastroenterology & hepatologyDNA mismatch repairFemaleMutL Protein Homolog 1geenitutkimusAdenomaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdenoma3122 CancersAdenomatous Polyposis Coli ProteinINSTABILITYSOCIETYMLH103 medical and health sciencesInternal medicinemedicineMANAGEMENTHumansLynchin oireyhtymäneoplasmspaksusuolisyöpäHepatologybusiness.industryCancernutritional and metabolic diseasesennusteetmedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesMSH6030104 developmental biologyMSH2Mutationbusiness
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Polymorphism of the Transcription Factor 7-Like 2 Gene (TCF7L2) Interacts with Obesity on Type-2 Diabetes in the PREDIMED Study Emphasizing the Heter…

2016

Nutrigenetic studies analyzing gene-diet interactions of the TCF7L2-rs7903146 C > T polymorphism on type-2 diabetes (T2D) have shown controversial results. A reason contributing to this may be the additional modulation by obesity. Moreover, TCF7L2-rs7903146 is one of the most influential variants in T2D-genetic risk scores (GRS). Therefore, to increase the predictive value (PV) of GRS it is necessary to first see whether the included polymorphisms have heterogeneous effects. We comprehensively investigated gene-obesity interactions between the TCF7L2-rs7903146 C > T polymorphism on T2D (prevalence and incidence) and analyzed other T2D-polymorphisms in a sub-sample. We studied 7018 PREDIMED …

0301 basic medicineOncologyMaleobesityendocrine system diseasesType 2 diabetestype-2 diabetesTranscription Factor 7-Like 2Dieta mediterrània0302 clinical medicineNutrigenomicsRisk FactorsPrevalenceTCF7L2-predictive valueDiseaseLongitudinal StudiesProspective StudiesGenetic riskGeneticsAged 80 and overINSULIN-RESISTANCEBioquímica y tecnologíaNutrition and DieteticsDiabetisIncidenceMiddle AgedTraitsMEDITERRANEAN DIETBiochemistry and technologyObesitatTRIALFemalelcsh:Nutrition. Foods and food supplyTranscription Factor 7-Like 2 ProteinAdultGenetic Markersmedicine.medical_specialtyendocrine systemPopulationBODY-FATlcsh:TX341-641030209 endocrinology & metabolismMASSBioquímica i biotecnologiaArticleAssociation03 medical and health sciencesGenetic HeterogeneityPredictive Value of TestsInternal medicineDiabetes mellitusmedicineHumansGenetic Predisposition to DiseaseGeneAgedPolymorphism Geneticbusiness.industryCommon variantsPreventionnutritional and metabolic diseasesGenetic VariationPREDIMED studymedicine.disease2072-6643WeightPredimedObesityTCF7L2TCF7L2; type-2 diabetes; obesity; T2D-genetic risk scores; TCF7L2-predictive value; PREDIMED study030104 developmental biologyDiabetes Mellitus Type 2Susceptibility locibusinessTCF7L2T2D-genetic risk scoresFood Science
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Impact of BMI on HER2+ metastatic breast cancer patients treated with pertuzumab and/or trastuzumab emtansine. Real-world evidence

2020

Body mass index (BMI) is a main indicator of obesity and its association with breast cancer is well established. However, little is known in the metastatic setting, especially in HER2-positive patients. We assessed the influence of BMI on clinical outcomes of patients treated with pertuzumab and/or trastuzumab emtansine (T-DM1) for HER2+ metastatic breast cancer (mBC). BMI was addressed as a categorical variable, being classified on the basis of the following ranges, that is, 18.5-24.9, 25-29.9, and 30.0-34.9, namely, normal weight, overweight, and Class I obesity. The outcomes chosen were progression-free survival to first-line chemotherapy (PFS1) and overall survival (OS). Overall (N = 70…

0301 basic medicineOncologyPhysiologyReceptor ErbB-2Clinical BiochemistryAdo-Trastuzumab EmtansineSettore MED/06body mass index; HER2-positive metastatic breast cancer; pertuzumab; trastuzumab emtansinechemistry.chemical_compound0302 clinical medicineAntineoplastic Agents ImmunologicalAged 80 and overeducation.field_of_studyUnivariate analysisMiddle AgedMetastatic breast cancerProgression-Free SurvivalQuartile030220 oncology & carcinogenesisHER2-positive metastatic breast cancerDisease ProgressionFemalePertuzumabmedicine.drugAdultmedicine.medical_specialtyPopulationBreast Neoplasmsbody mass indexAntibodies Monoclonal Humanized03 medical and health sciencesBreast cancerSettore MED/04 - PATOLOGIA GENERALEpertuzumabInternal medicinemedicineHumansObesityeducationAgedtrastuzumab emtansinebusiness.industrynutritional and metabolic diseasesCell BiologyOverweightmedicine.disease030104 developmental biologychemistryTrastuzumab emtansineMED/06 - ONCOLOGIA MEDICAbusinessBody mass index
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