Search results for "nutritional and metabolic diseases"

showing 10 items of 673 documents

Sugar-sweetened and artificially-sweetened beverages and changes in cognitive function in the SUN project.

2019

Background: Sugar-sweetened beverages (SSB) and artificially-sweetened beverages (ASB) have been inconsistently associated with declines in cognitive function. Because of their low caloric content ...

0301 basic medicineMaleMedicine (miscellaneous)Neuropsychological Tests03 medical and health sciences0302 clinical medicineCognitionmedicineDementiaHumansCognitive DysfunctionFood scienceLongitudinal StudiesProspective StudiesSugarAgedSugar-Sweetened Beverages030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryGeneral Neurosciencedigestive oral and skin physiologyArtificially Sweetened Beveragesnutritional and metabolic diseasesfood and beveragesCaloric theoryCognitionGeneral MedicineMiddle Agedmedicine.diseasestomatognathic diseasesSpainbusinesshuman activities030217 neurology & neurosurgeryNutritional neuroscience
researchProduct

A possible role of FANCM mutations in male breast cancer susceptibility: Results from a multicenter study in Italy

2018

Abstract Introduction Breast cancer (BC) in men is a rare disease, whose etiology appears to be associated with genetic factors. Inherited mutations in BRCA1/2 genes account for about 10–15% of all cases. FANCM, functionally linked to BRCA1/2, has been suggested as a novel BC susceptibility gene. Our aim was to test if FANCM germline mutations could further explain male BC (MBC) susceptibility. Methods We screened the entire coding region of FANCM in 286 MBCs by a multi-gene panel analysis, and compared these data with available whole exome sequencing data from 415 men used as population controls. Moreover, we genotyped the two most frequent FANCM mutations (c.5101C>T and c.5791C>T) in 506 …

0301 basic medicineMaleMutation rateSettore MED/06 - Oncologia MedicaDNA Helicasemedicine.disease_causeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; Adult; Aged; Aged 80 and over; Biomarkers Tumor; Breast Neoplasms Male; Case-Control Studies; DNA Helicases; Genetic Predisposition to Disease; Genotype; Germ-Line Mutation; Humans; Italy; Male; Middle Aged; Risk Factors; Whole Genome Sequencing; Young Adult; Surgery0302 clinical medicineFANCMRisk Factorshemic and lymphatic diseasesGermline mutationGenotypeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; SurgeryFANCMMutation frequencyGeneticsAged 80 and overeducation.field_of_studyMutationGeneral MedicineMiddle AgedItaly030220 oncology & carcinogenesisMale breast cancerCase-Control StudieHumanAdultcongenital hereditary and neonatal diseases and abnormalitiesGenotypePopulationBreast Neoplasms Male03 medical and health sciencesYoung AdultGermline mutationBRCA1/2medicineBiomarkers TumorHumansGenetic Predisposition to DiseaseeducationGermline mutationsGerm-Line MutationAgedBreast cancer susceptibilityWhole Genome Sequencingbusiness.industryRisk FactorDNA Helicasesnutritional and metabolic diseasesmedicine.diseaseMale breast cancer030104 developmental biologyCase-Control StudiesSurgerybusiness
researchProduct

Simultaneous Inhibition of Peripheral CB1R and iNOS Mitigates Obesity-Related Dyslipidemia Through Distinct Mechanisms.

2020

Diabetic dyslipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol levels, is a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in type 2 diabetes. Activation of the cannabinoid-1 receptor (CB1R) and activation of inducible nitric oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis progression. Here, we tested whether dual-targeting inhibition of hepatic CB1R and iNOS improves diabetic dyslipidemia in mice with diet-induced obesity (DIO mice). DIO mice were treated for 14 days with (S)-MRI-1867, a peripherally restricted hybrid inhibitor of CB1R and iNOS. (R)-MRI-1867, the CB1R-inactive stereoisomer that …

0301 basic medicineMaleVery low-density lipoproteinEndocrinology Diabetes and MetabolismNitric Oxide Synthase Type II[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB][SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMice0302 clinical medicineReceptor Cannabinoid CB1[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Receptor[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismbiology[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Nitric oxide synthaseLiver[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyKexinlipids (amino acids peptides and proteins)medicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]LipoproteinsImmunoblotting030209 endocrinology & metabolismReal-Time Polymerase Chain Reaction03 medical and health sciencesInternal medicineCommentariesInternal MedicinemedicineAnimalsObesity[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Dyslipidemiasbusiness.industry[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]PCSK9nutritional and metabolic diseases[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseLipid Metabolism[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseLDL receptorbiology.proteinHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologySteatosisbusinessDyslipidemia
researchProduct

Differential Impact of Ad Libitum or Intermittent High-Fat Diets on Bingeing Ethanol-Mediated Behaviors

2019

Background: Dietary factors have significant effects on the brain, modulating mood, anxiety, motivation and cognition. To date, no attention has been paid to the consequences that the combination of ethanol (EtOH) and a high-fat diet (HFD) have on learning and mood disorders during adolescence. The aim of the present work was to evaluate the biochemical and behavioral consequences of ethanol binge drinking and an HFD consumption in adolescent mice. Methods: Animals received either a standard diet or an HFD (ad libitum vs. binge pattern) in combination with ethanol binge drinking and were evaluated in anxiety and memory. The metabolic profile and gene expression of leptin receptors and clock…

0301 basic medicineMalecognitionHippocampusCLOCK ProteinsWhite adipose tissueWeight GainHippocampusMice0302 clinical medicineBulimiaPrefrontal cortexAdiposityNutrition and DieteticsLeptindigestive oral and skin physiologyARNTL Transcription Factorsfood and beveragesanxietyhigh-fat dietReceptors Leptinlcsh:Nutrition. Foods and food supplyhormones hormone substitutes and hormone antagonistsmedicine.medical_specialtymedicine.drug_classBinge drinkingPrefrontal Cortexlcsh:TX341-641Diet High-FatAnxiolyticleptinArticle03 medical and health sciencesInternal medicinemedicineAnimalsLearningLeptin receptorEthanolbusiness.industryMood Disordersnutritional and metabolic diseasesmedicine.diseasebinge drinking030104 developmental biologyEndocrinologyMood disordersgene expressionbusiness030217 neurology & neurosurgeryFood Science
researchProduct

Whole-blood transcriptome profiling reveals signatures of metformin and its therapeutic response

2020

Metformin, a biguanide agent, is the first-line treatment for type 2 diabetes mellitus due to its glucose-lowering effect. Despite its wide application in the treatment of multiple health conditions, the glycemic response to metformin is highly variable, emphasizing the need for reliable biomarkers. We chose the RNA-Seq-based comparative transcriptomics approach to evaluate the systemic effect of metformin and highlight potential predictive biomarkers of metformin response in drug-naive volunteers with type 2 diabetes in vivo. The longitudinal blood-derived transcriptome analysis revealed metformin-induced differential expression of novel and previously described genes involved in cholester…

0301 basic medicineMaleendocrine system diseasesMolecular biologyGene ExpressionType 2 diabetesPharmacologyBiochemistryTranscriptome0302 clinical medicineEndocrinologyMedical ConditionsSequencing techniquesGastrointestinal CancersBreast TumorsMedicine and Health SciencesHomeostasisEnergy-Producing OrganellesWhole bloodMultidisciplinarySmall nuclear RNABiguanideQRRNA sequencingGenomicsMiddle AgedMetforminMetforminMitochondriaType 2 DiabetesNucleic acidsCholesterolSmall nucleolar RNAOncology030220 oncology & carcinogenesisMedicineFemaleCellular Structures and OrganellesTranscriptome Analysismedicine.drugResearch Articlemedicine.drug_classEndocrine DisordersScienceGastroenterology and HepatologyBioenergetics03 medical and health sciencesBreast CancermedicineGeneticsDiabetes MellitusHumansNon-coding RNAGlycemicAgedbusiness.industryGene Expression ProfilingType 2 Diabetes Mellitusnutritional and metabolic diseasesBiology and Life SciencesComputational BiologyCancers and NeoplasmsCell Biologymedicine.diseaseGenome AnalysisGene regulationGene expression profilingResearch and analysis methods030104 developmental biologyMolecular biology techniquesMetabolic DisordersRNAbusinessBlood Chemical AnalysisPLoS ONE
researchProduct

Neuroprotective potential of antihyperglycemic drug metformin in streptozocin-induced rat model of sporadic Alzheimer's disease.

2020

Abstract The earliest hallmarks of sporadic Alzheimer's disease (sAD) are impaired glucose metabolism, chronic neuroinflammation, diminished synaptic plasticity and subsequent cognitive decline. The safest antidiabetic drug metformin has shown both glucose metabolism-improving and cognition-enhancing action in type 2 diabetes patients and diabetic model animals. However, metformin has not been previously studied in intracerebroventricular streptozocin (STZ)-induced model of sAD. Therefore, our aim was to assess the preventive action of metformin in sAD model-rats. Firstly, the actions of metformin (75 and 100 mg/kg) on cognitive functions and sociability were examined. Secondly, we wanted t…

0301 basic medicineMaleendocrine system diseasesNerve Tissue ProteinsType 2 diabetesPharmacologyGPI-Linked ProteinsNeuroprotectionStreptozocin03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCognitionAlzheimer DiseaseMorris Water Maze TestMedicineAnimalsHypoglycemic AgentsCognitive declineRats WistarSocial BehaviorNeuroinflammationInjections IntraventricularPharmacologyGlucose Transporter Type 1Behavior AnimalGlucose Transporter Type 3business.industrydigestive oral and skin physiologyGlucose transporternutritional and metabolic diseasesBrainmedicine.diseaseMetforminMetforminAstrogliosisDisease Models Animal030104 developmental biologyGlucoseNeuroprotective AgentsSynaptic plasticityAcetylcholinesterasebusinessNeuroglia030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
researchProduct

A Network Involving Gut Microbiota, Circulating Bile Acids, and Hepatic Metabolism Genes That Protects Against Non-Alcoholic Fatty Liver Disease.

2019

Scope Gut microbiota contributes to non-alcoholic fatty liver disease (NAFLD) pathogenesis by multiple mechanisms not yet completely understood. Novel differential features between germ-free mice (GFm) transplanted with protective or non-protective cecal microbiota against NAFLD are investigated. Methods and results Gut microbiota composition, plasma, and fecal bile acids (BAs) and liver mRNAs are quantified in GFm recipients from four donor mice differing in NAFLD severity (control diet, high-fat diet [HFD]-responder, HFD-non-responder, and quercetin-supplemented HFD). Transplanted GFm are on control or HFD for 16-weeks. Multivariate analysis shows that GFm colonized with microbiota from H…

0301 basic medicineMalemedicine.medical_specialtyGut floraDiet High-Fatdigestive systemPathogenesisBile Acids and Salts03 medical and health sciencesMiceNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsFeces030109 nutrition & dieteticsbiologyEthanoldigestive oral and skin physiologyFatty livernutritional and metabolic diseasesTransporterbiology.organism_classificationmedicine.diseasePhenotypeGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologyLiverBacteroidesTranscriptomeDrug metabolismFood ScienceBiotechnologyMolecular nutritionfood research
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct