Search results for "glycemia"

showing 10 items of 159 documents

Activation of PPARβ/δ prevents hyperglycaemia-induced impairment of Kv7 channels and cAMP-mediated relaxation in rat coronary arteries.

2016

PPARβ/δ activation protects against endothelial dysfunction in diabetic models. Elevated glucose is known to impair cAMP-induced relaxation and Kv channel function in coronary arteries (CA). Herein, we aimed to analyse the possible protective effects of the PPARβ/δ agonist GW0742 on the hyperglycaemic-induced impairment of cAMP-induced relaxation and Kv channel function in rat CA. As compared with low glucose (LG), incubation under high glucose (HG) conditions attenuated the relaxation induced by the adenylate cyclase activator forskolin in CA and this was prevented by GW0742. The protective effect of GW0742 was supressed by a PPARβ/δ antagonist. In myocytes isolated from CA under LG, forsk…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPDK4Protein Serine-Threonine Kinasesmedicine.disease_causeGW0742Diabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineCyclic AMPAnimalsHumansPPAR deltaRats WistarPPAR-betaForskolinAntagonistPyruvate Dehydrogenase Acetyl-Transferring KinaseGeneral MedicineHyperpolarization (biology)Coronary VesselsPotassium channelRatsVasodilationThiazoles030104 developmental biologyEndocrinologychemistryHyperglycemiaKCNQ1 Potassium ChannelReactive Oxygen SpeciesOxidative stressClinical science (London, England : 1979)
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Direct Sensing of Nutrients via a LAT1-like Transporter in Drosophila Insulin-Producing Cells

2016

Summary Dietary leucine has been suspected to play an important role in insulin release, a hormone that controls satiety and metabolism. The mechanism by which insulin-producing cells (IPCs) sense leucine and regulate insulin secretion is still poorly understood. In Drosophila, insulin-like peptides (DILP2 and DILP5) are produced by brain IPCs and are released in the hemolymph after leucine ingestion. Using Ca2+-imaging and ex vivo cultured larval brains, we demonstrate that IPCs can directly sense extracellular leucine levels via minidiscs (MND), a leucine transporter. MND knockdown in IPCs abolished leucine-dependent changes, including loss of DILP2 and DILP5 in IPC bodies, consistent wit…

0301 basic medicineAmino Acid Transport Systemsheavy-chainmedicine.medical_treatmentInsulinsamino acid transporter0302 clinical medicinegenetics [Drosophila Proteins]cytology [Drosophila melanogaster]Glutamate DehydrogenaseHemolymphInsulin-Secreting Cellsmetabolism [Drosophila melanogaster]HemolymphDrosophila;Drosophila insulin-like peptides;amino acid transporter;food;glutamate dehydrogenase;glycemia;growth;insulin-producing cells;minidiscs;starvationDrosophila ProteinsProtein Isoformsmetabolism [Calcium]genetics [Insulins]genetics [Amino Acid Transport Systems]lcsh:QH301-705.5minidiscsGene knockdowncytology [Larva]pancreatic beta-cellglutamate dehydrogenaseBrainmetabolism [Hemolymph]secretionDrosophila melanogasterBiochemistryLarvaAlimentation et NutritionDrosophilaLeucineSignal Transductionglucose-transportgenetics [Glutamate Dehydrogenase]genetics [Protein Isoforms]growthamino-acidsmetabolism [Drosophila Proteins][SDV.BC]Life Sciences [q-bio]/Cellular BiologyNutrient sensingmetabolism [Larva]Biologyinsulin-producing cellsArticleGeneral Biochemistry Genetics and Molecular Biologymetabolism [Amino Acid Transport Systems]metabolism [Insulins]03 medical and health sciencesLeucineparasitic diseasesmedicineFood and NutritionAnimalsddc:610cytology [Insulin-Secreting Cells]cardiovascular diseasesAmino acid transporterMnd protein Drosophilaadministration & dosage [Leucine]metabolism [Protein Isoforms]Ilp5 protein Drosophilacytology [Brain]foodGlutamate dehydrogenaseInsulinNeurosciencesstarvationGlucose transportermetabolism [Insulin-Secreting Cells]glutamate-dehydrogenasel-leucineglycemia030104 developmental biologyGene Expression Regulationlcsh:Biology (General)metabolism [Brain]metabolism [Glutamate Dehydrogenase]Neurons and Cognitionmetabolism [Leucine]CalciumDrosophila insulin-like peptidesmetabolismfat-cells030217 neurology & neurosurgeryCell Reports
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Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
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Prevalence and determinants of non-alcoholic fatty liver disease in lifelines: A large Dutch population cohort

2017

BACKGROUND & AIMS Non-alcoholic fatty liver disease is an increasing health issue that develops rather unnoticed with obesity, type 2 diabetes mellitus and metabolic syndrome. We investigated prevalence, determinants and associated metabolic abnormalities of non-alcoholic fatty liver disease in the largest population-based cohort to date. METHODS Biochemical characteristics, type 2 diabetes mellitus and metabolic syndrome were determined in the Lifelines Cohort Study (N = 167,729), a population-based cohort in the North of the Netherlands. Non-alcoholic fatty liver disease was defined as Fatty Liver Index (FLI)≥60. Exclusion criteria were age <18 years, immigrants, missing data to assess FL…

0301 basic medicineMaleCirrhosislcsh:MedicineGastroenterologyBiochemistryGLOMERULAR-FILTRATION-RATESTEATOHEPATITISWhite Blood Cells0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsAnimal CellsPrevalenceMedicine and Health SciencesDiabetes diagnosis and managementlcsh:ScienceNetherlandsMETABOLIC SYNDROME2. Zero hungerINSULIN-RESISTANCEMultidisciplinaryLiver DiseasesFatty liverMiddle AgedLipids3. Good healthType 2 DiabetesCholesterolHypertension030211 gastroenterology & hepatologyFemaleAnatomyCellular TypesResearch ArticleAdultmedicine.medical_specialtyHbA1cEndocrine DisordersImmune CellsImmunologyUNITED-STATESGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansHemoglobinHEPATIC STEATOSISHepatitisBlood Cellsbusiness.industryCholesterol HDLlcsh:RType 2 Diabetes MellitusBiology and Life SciencesProteinsRenal SystemCell Biologymedicine.diseaseDiagnostic medicineFatty LiverSERUM CREATININE VALUESRENAL-DISEASE030104 developmental biologyEndocrinologyCross-Sectional StudiesDiabetes Mellitus Type 2ATHEROSCLEROSISHyperglycemiaMetabolic DisordersRISK-FACTORSlcsh:QSteatohepatitisMetabolic syndromebusiness
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Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycae…

2016

Extracellular vesicles (EVs) that are derived from stem cells are proving to be promising therapeutic options. We herein investigate the therapeutic potential of EVs that have been derived from different stem cell sources, bone-marrow (MSC) and human liver (HLSC), on mesangial cells (MCs) exposed to hyperglycaemia. By expressing a dominant negative STAT5 construct (ΔNSTAT5) in HG-cultured MCs, we have demonstrated that miR-21 expression is under the control of STAT5, which translates into Transforming Growth Factor beta (TGFβ) expression and collagen production. A number of approaches have been used to show that both MSC- and HLSC-derived EVs protect MCs from HG-induced damage via the trans…

0301 basic medicineMolecular biologyCellGene Expressionlcsh:MedicineBiochemistry0302 clinical medicineAnimal CellsChronic Kidney DiseaseMedicine and Health SciencesSTAT5 Transcription FactorRNA Processing Post-Transcriptionallcsh:ScienceSTAT5Energy-Producing OrganellesCells CulturedMultidisciplinarybiologyMesangial cellStem CellsVector ConstructionCell biologyMitochondriaEnzymesmedicine.anatomical_structureBiochemistryNephrology030220 oncology & carcinogenesisMesangial CellsCollagenStem cellCellular TypesCellular Structures and OrganellesOxidoreductasesLuciferaseResearch ArticleCollagen Type IVBioenergeticsDNA constructionModels Biological03 medical and health sciencesExtracellular VesiclesmicroRNAmedicineGene Expression and Vector TechniquesGeneticsHumansVesiclesCell ProliferationMolecular Biology Assays and Analysis TechniquesCell growthMesenchymal stem celllcsh:RBiology and Life SciencesProteinsMesenchymal Stem CellsTransforming growth factor betaCell BiologyResearch and analysis methodsMicroRNAs030104 developmental biologyMolecular biology techniquesGlucoseHyperglycemiabiology.proteinEnzymologylcsh:QCollagensPLoS ONE
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Diabetic macroangiopathy: Pathogenetic insights and novel therapeutic approaches with focus on high glucose-mediated vascular damage

2018

Diabetic macroangiopathy - a specific form of accelerated atherosclerosis - is characterized by intra-plaque new vessel formation due to excessive/abnormal neovasculogenesis and angiogenesis, increased vascular permeability of the capillary vessels, and tissue edema, resulting in frequent atherosclerotic plaque hemorrhage and plaque rupture. Mechanisms that may explain the premature and rapidly progressive nature of atherosclerosis in diabetes are multiple, and to a large extent still unclear. However, mechanisms related to hyperglycemia certainly play an important role. These include a dysregulated vascular regeneration. In addition, oxidative and hyperosmolar stresses, as well as the acti…

0301 basic medicineProteomicsPhysiologyAngiogenesisAquaporinMetabolomicVascular permeability030204 cardiovascular system & hematologyDiabeteBioinformaticsAquaporins03 medical and health sciences0302 clinical medicineDiabetes mellitusMedicineMetabolomicsMacrovascular diseasePharmacologybusiness.industryAquaporinRegeneration (biology)DiabetesPlaque rupturemedicine.diseaseAtherosclerosisAquaporins; Atherosclerosis; Diabetes; Hyperglycemia; Metabolomics; Proteomics030104 developmental biologyAtherosclerosiHyperglycemiaHigh glucoseMolecular Medicinebusiness
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Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy

2017

Fasting reduces glucose levels and protects mice against chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment. Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (DXR). Such toxicity can be reversed by reducing circulating glucose levels by fasting or insulin. Furthermore, glucose injections alone reversed the fasting-dependent protection against DXR in mice, indicating that elevated glucose mediates, at least in part, the sensitizing effects of rapamycin and dexamethasone. In yeast, glucose activates protein kinase A (P…

0301 basic medicineTime FactorsImmunology and Microbiology (all)Peptide Hormonesmedicine.medical_treatmentAMP-Activated Protein KinasesToxicologyPathology and Laboratory MedicineBiochemistryDexamethasoneMiceEndocrinologyAMP-activated protein kinaseAtrial natriuretic peptideNatriuretic Peptide BrainMedicine and Health SciencesNatriuretic peptideInsulinSmall interfering RNAsBiology (General)Statistical DatabiologyOrganic CompoundsGeneral NeuroscienceMonosaccharidesHeartFastingMetformin3. Good healthMetforminNucleic acidsChemistryPhysical SciencesFemaleAnatomyGeneral Agricultural and Biological SciencesStatistics (Mathematics)Atrial Natriuretic FactorResearch Articlemedicine.drugmedicine.medical_specialtyQH301-705.5medicine.drug_classCarbohydratesEGR1Antineoplastic AgentsCardiotoxinsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesNatriuretic PeptideStress PhysiologicalInternal medicineGeneticsmedicineAnimalsNon-coding RNAProtein kinase AEarly Growth Response Protein 1Diabetic EndocrinologyNeuroscience (all)Biochemistry Genetics and Molecular Biology (all)Biology and life sciencesToxicityGeneral Immunology and MicrobiologyInsulinOrganic ChemistryChemical CompoundsCorrectionAMPKCyclic AMP-Dependent Protein KinasesHormonesGene regulationDietAtrial Natriuretic PeptideMice Inbred C57BLNeuroscience (all); Immunology and Microbiology (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Glucose030104 developmental biologyEndocrinologyAgricultural and Biological Sciences (all)CytoprotectionMetabolic DisordersHyperglycemiaCardiovascular Anatomybiology.proteinRNAGene expressionMathematicsPLOS Biology
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Expert opinion on the metabolic complications of mTOR inhibitors

2018

Abstract Using mTOR inhibitors (mTORi) as anticancer drugs led to hyperglycemia (12–50%) and hyperlipidemia (7–73%) in phase-III trials. These high rates require adapted treatment in cancer patients. Before initiating mTORi treatment, lipid profile screening should be systematic, with fasting glucose assay in non-diabetic patients and HbA1C in diabetic patients. After initiation, lipid profile monitoring should be systematic, with fasting glucose assay in non-diabetic patients, every 2 weeks for the first month and then monthly. The HbA1C target is ≤ 8%, before and after treatment initiation in known diabetic patients and in case of onset of diabetes under mTORi. LDL-cholesterol targets sho…

0301 basic medicinemedicine.medical_specialtyConsensusEndocrinology Diabetes and MetabolismAtorvastatinAntineoplastic Agents03 medical and health sciences0302 clinical medicineEndocrinologyMetabolic DiseasesNeoplasmsInternal medicineDiabetes mellitusHyperlipidemiamedicineHumansDyslipidemiasFenofibratemedicine.diagnostic_testbusiness.industryTOR Serine-Threonine KinasesHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseHypoglycemia030104 developmental biologySimvastatin030220 oncology & carcinogenesislipids (amino acids peptides and proteins)Lipid profilebusinessPravastatinmedicine.drugAnnales d'Endocrinologie
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Long-Term Aspartame Administration Leads to Fibrosis, Inflammasome Activation, and Gluconeogenesis Impairment in the Liver of Mice

2021

Background: Aspartame is an artificial sweetener used in foods and beverages worldwide. However, it is linked to oxidative stress, inflammation, and liver damage through mechanisms that are not fully elucidated yet. This work aimed to investigate the effects of long-term administration of aspartame on the oxidative and inflammatory mechanisms associated with liver fibrosis progression in mice. Methods: Mice were divided into two groups with six animals each: control and aspartame. Aspartame (80 mg/kg, via oral) or vehicle was administrated for 12 weeks. Results: Aspartame caused liver damage and elevated serum transaminase levels. Aspartame also generated liver fibrosis, as evidenced by his…

0301 basic medicinemedicine.medical_specialtyPGC-1αInflammationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyArticleaspartameNrf2Lipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationFibrosislipidinflammasomeInternal medicinemedicinelcsh:QH301-705.5liver fibrosisGeneral Immunology and MicrobiologyAspartameInflammasomelipid peroxidationmedicine.diseaseCollagen type I alpha 1030104 developmental biologyEndocrinologyhypoglycemiagluconeogenesischemistrylcsh:Biology (General)030211 gastroenterology & hepatologymedicine.symptomGeneral Agricultural and Biological SciencesOxidative stressmedicine.drugBiology
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The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperg…

2019

Background/aims Mitochondria-targeted antioxidants such as mitoquinone (MitoQ) have demonstrated protective effects against oxidative damage in several diseases. The increase in reactive oxygen species (ROS) production during glucose metabolism in β cells can be exacerbated under hyperglycaemic conditions such as type 2 diabetes (T2D), thus contributing to β cell function impairment. In the present work, we aimed to evaluate the effect of MitoQ on insulin secretion, oxidative stress, endoplasmic reticulum (ER) stress and nuclear factor kappa B (NFκB) signalling in a pancreatic β cell line under normoglycaemic (NG, 11.1 mM glucose), hyperglycaemic (HG, 25 mM glucose) and lipidic (palmitic ac…

0301 basic medicinemedicine.medical_specialtyPhysiologyUbiquinoneCarbohydrate metabolismmedicine.disease_causeMitoQlcsh:PhysiologyPancreatic β cellsAntioxidantsProinflammatory cytokinelcsh:Biochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsInternal medicineCell Line TumorInsulin-Secreting CellsmedicineAnimalslcsh:QD415-436chemistry.chemical_classificationReactive oxygen speciesMitoQlcsh:QP1-981Endoplasmic reticulumGlutathioneEndoplasmic Reticulum StressType 2 DiabetesMitochondriaRatsOxidative Stress030104 developmental biologyEndocrinologyGlucosechemistry030220 oncology & carcinogenesisHyperglycemiaUnfolded protein responseER stressMitochondrial dysfunctionReactive Oxygen SpeciesOxidative stressSignal Transduction
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