Search results for "CHON"

showing 10 items of 1866 documents

Relationship between PMN-endothelium interactions, ROS production and Beclin-1 in type 2 diabetes.

2020

Type 2 diabetes is closely related to oxidative stress and cardiovascular diseases. In this study, we hypothesized that polymorphonuclear leukocytes (PMN)-endothelium interactions and autophagy are associated. We evaluated PMN-endothelial interactions, ROS production and autophagy parameters in 47 type 2 diabetic patients and 57 control subjects. PMNs from type 2 diabetic patients exhibited slower rolling velocity (p < 0.001), higher rolling flux (p < 0.001) and adhesion (p < 0.001) in parallel to higher levels of total (p < 0.05) and mitochondrial ROS (p < 0.05). When the protein expression of autophagy markers was analysed, an increase of Beclin-1 (p < 0.05), LC3I (p < 0.05), LC3II (p < 0…

0301 basic medicinemedicine.medical_specialtyEndotheliumNeutrophilsClinical BiochemistryType 2 diabetesMitochondrionmedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineInternal medicineDiabetes mellitusmedicineAutophagyCell AdhesionHumansEndotheliumlcsh:QH301-705.5lcsh:R5-920ChemistryOrganic ChemistryAutophagyRolling velocityType 2 diabetesROSmedicine.diseaseControl subjectsMitochondria030104 developmental biologymedicine.anatomical_structureEndocrinologylcsh:Biology (General)Diabetes Mellitus Type 2Oxidative stressCase-Control StudiesPMN-Endothelium interactionsBeclin-1lcsh:Medicine (General)Reactive Oxygen Species030217 neurology & neurosurgeryOxidative stressResearch PaperRedox biology
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Current disease modifying approaches to treat Parkinson's disease

2015

Parkinson's disease (PD is a progressive neurological disorder characterized by the degeneration and death of midbrain dopamine and non-dopamine neurons in the brain leading to motor dysfunctions and other symptoms, which seriously influence the quality of life of PD patients. The drug L-dopa can alleviate the motor symptoms in PD, but so far there are no rational therapies targeting the underlying neurodegenerative processes. Despite intensive research, the molecular mechanisms causing neuronal loss are not fully understood which has hampered the development of new drugs and disease-modifying therapies. Neurotrophic factors are by virtue of their survival promoting activities attract candi…

0301 basic medicinemedicine.medical_specialtyParkinson's diseaseNeurturinNeurotrophic factorBiologySettore BIO/09 - Fisiologia03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeuroinflammationDopamineNeurotrophic factorsInternal medicineα-SynucleinmedicineGlial cell line-derived neurotrophic factorMolecular BiologyCerebral dopamine neurotrophic factorDopamine neuronPharmacologyDopaminergicCell Biologymedicine.diseaseDopamine neurons; ER stress; Mitochondria; Neuroinflammation; Neuropeptides; Neurotrophic factors; Protein aggregation; α-Synuclein; Molecular Medicine; Molecular Biology; Pharmacology; Cellular and Molecular Neuroscience; Cell Biology3. Good healthMitochondriaNeuropeptide030104 developmental biologyNerve growth factorEndocrinologybiology.proteinER streMolecular MedicineProtein aggregationNeuroscience030217 neurology & neurosurgerymedicine.drug
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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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Obesogenic Diets Cause Alterations on Proteins and Theirs Post-Translational Modifications in Mouse Brains

2021

Obesity constitutes a major global health threat and is associated with a variety of diseases ranging from metabolic and cardiovascular disease, cancer to neurodegeneration. The hallmarks of neurodegeneration include oxidative stress, proteasome impairment, mitochondrial dysfunction and accumulation of abnormal protein aggregates as well as metabolic alterations. As an example, in post-mortem brain of patients with Alzheimer’s disease (AD), several studies have reported reduction of insulin, insulin-like growth factor 1 and insulin receptor and an increase in tau protein and glycogen-synthase kinase-3β compared to healthy controls suggesting an impairment of metabolism in the AD patient’s …

0301 basic medicinemedicine.medical_specialtyRC620-627Endocrinology Diabetes and Metabolismmedicine.medical_treatmentTau proteinObesity nutrition brain impairment proteomics post-translational modificationsBrain damageMitochondrionProteomicsmedicine.disease_causeSettore BIO/09 - Fisiologia03 medical and health sciencesproteomics0302 clinical medicineInternal medicinepost-translational modificationsmedicineTX341-641ObesityNutritional diseases. Deficiency diseasesOriginal ResearchSettore MED/04 - Patologia GeneraleNutrition and DieteticsbiologyNutrition. Foods and food supplyInsulinNeurodegenerationmedicine.diseasebrain impairmentInsulin receptornutrition030104 developmental biologyEndocrinologybiology.proteinmedicine.symptom030217 neurology & neurosurgeryOxidative stressFood ScienceNutrition and Metabolic Insights
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Olesoxime improves cerebral mitochondrial dysfunction and enhances Aβ levels in preclinical models of Alzheimer's disease.

2019

Abstract Background Approved drugs for Alzheimer's disease (AD) only have a symptomatic effects and do not intervene causally in the course of the disease. Olesoxime (TRO19622) has been tested in AD disease models characterized by improved amyloid precursor protein processing (AβPP) and mitochondrial dysfunction. Methods Three months old Thy-1-AβPPSL (tg) and wild type mice (wt) received TRO19622 (100 mg/kg b.w.) in supplemented food pellets for 15 weeks (tg TRO19622). Mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) levels were determined in dissociated brain cells (DBC). Respiration was analyzed in mitochondria isolated from brain tissue. Citrate synthase (CS) activ…

0301 basic medicinemedicine.medical_specialtyRespiratory chainMice TransgenicMitochondrionLipid peroxidation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeuroscienceAlzheimer DiseaseInternal medicineMembrane fluidityAmyloid precursor proteinmedicineCitrate synthaseAnimalsHumansCholestenonesAmyloid beta-PeptidesbiologyBrainRotenoneMitochondriaMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyHEK293 CellsNeurologychemistrybiology.proteinOlesoximeFemale030217 neurology & neurosurgeryExperimental neurology
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Atorvastatin but not pravastatin impairs mitochondrial function in human pancreatic islets and rat β-cells. Direct effect of oxidative stress

2017

AbstractStatins are a class of drugs widely prescribed as frontline therapy for lowering plasma LDL-cholesterol in cardiovascular risk prevention. Several clinical reports have recently suggested an increased risk of type 2 diabetes associated with chronic use of these drugs. The pathophysiology of this effect remains to be fully elucidated but impaired β-cell function constitutes a potential mechanism. The aim of this study was to explore the effect of a chronic treatment with lipophilic and hydrophilic statins on β-cell function, using human pancreatic islets and rat insulin-secreting INS-1 cells; we particularly focused on the role of mitochondria and oxidative stress. The present study …

0301 basic medicinemedicine.medical_specialtyStatinmedicine.drug_classmedicine.medical_treatmentAtorvastatinPancreatic isletslcsh:MedicineType 2 diabetes030204 cardiovascular system & hematologyMitochondrionPharmacologymedicine.disease_causeArticle03 medical and health sciences0302 clinical medicineInternal medicinemedicinelcsh:ScienceMultidisciplinarybusiness.industryPancreatic isletsInsulinlcsh:RStatinmedicine.disease030104 developmental biologyEndocrinologymedicine.anatomical_structurelcsh:Qlipids (amino acids peptides and proteins)Statins; Pancreatic isletsbusinessOxidative stressPravastatinmedicine.drug
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Resveratrol Interferes with IL1-β-Induced Pro-Inflammatory Paracrine Interaction between Primary Chondrocytes and Macrophages

2016

International audience; State of the art. Osteoarthritis (OA) is a chronic articular disease characterized by cartilage degradation and osteophyte formation. OA physiopathology is multifactorial and involves mechanical and hereditary factors. So far, there is neither preventive medicine to delay cartilage breakdown nor curative treatment. Objectives. To investigate pro-inflammatory paracrine interactions between human primary chondrocytes and macrophages following interleukin-1-β (IL-1β) treatment; to evaluate the molecular mechanism responsible for the inhibitory effect of resveratrol. Results. The activation of NF-κB in chondrocytes by IL-1β induced IL-6 secretion. The latter will then ac…

0301 basic medicinemedicine.medical_specialtyTime Factors[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betalcsh:TX341-641InflammationmacrophageResveratrolresveratrolChondrocyteArticleNF-κBSTAT303 medical and health scienceschemistry.chemical_compoundParacrine signallingChondrocytesInternal medicineStilbenesmedicineMacrophageHumansSecretionCells CulturedInflammationNutrition and DieteticsCartilageMacrophagesAnti-Inflammatory Agents Non-SteroidalNF-κBIL1-β; chondrocyte; macrophage; NF-κB; STAT3; resveratrolCoculture TechniquesCell biology030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistrychondrocytemedicine.symptomIL1-βlcsh:Nutrition. Foods and food supplyBiomarkersFood ScienceNutrients
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Can mild cognitive impairment be stabilized by showering brain mitochondria with laser photons?

2019

There is now substantial evidence that cerebral blood flow (CBF) declines with age. From age 20 to 60, CBF is estimated to dip about 16% and continues to drop at a rate of 0.4%/year. This CBF dip will slowly reduce oxygen/glucose delivery to brain thus lowering ATP energy production needed by brain cells to perform normal activities. Reduced ATP production from mitochondrial loss or damage in the wear-and-tear of aging worsens when vascular risk factors (VRF) to Alzheimer's disease develop that can accelerate both age-decline CBF and mitochondrial deficiency to a level where mild cognitive impairment (MCI) develops. To date, no pharmacological or any other treatment has been successful in r…

0301 basic medicinemedicine.medical_specialtyTraumatic brain injuryDiseaseBrain mitochondria03 medical and health sciencesCellular and Molecular NeuroscienceTherapeutic approach0302 clinical medicineInternal medicineMedicineAging brainHumansCognitive DysfunctionCognitive impairmentPharmacologyPhotonsbusiness.industryBrainmedicine.diseaseMitochondria030104 developmental biologyCerebral blood flowBrain stimulationCardiologyLaser Therapybusiness030217 neurology & neurosurgeryNeuropharmacology
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Mitochondrial DNA Haplogroup JT is Related to Impaired Glycaemic Control and Renal Function in Type 2 Diabetic Patients

2018

The association between mitochondrial DNA (mtDNA) haplogroup and risk of type 2 diabetes (T2D) is undetermined and controversial. This study aims to evaluate the impact of the main mtDNA haplogroups on glycaemic control and renal function in a Spanish population of 303 T2D patients and 153 healthy controls. Anthropometrical and metabolic parameters were assessed and mtDNA haplogroup was determined in each individual. Distribution of the different haplogroups was similar in diabetic and healthy populations and, as expected, T2D patients showed poorer glycaemic control and renal function than controls. T2D patients belonging to the JT haplogroup (polymorphism m.4216T&gt

0301 basic medicinemedicine.medical_specialtyendocrine system diseasesgenetic structurestype 2 diabetes mellituslcsh:MedicineRenal functionType 2 diabetesArticleHaplogroupNephropathyDiabetic nephropathy03 medical and health scienceschemistry.chemical_compoundInternal medicineMedicineCreatininebusiness.industrymtDNAlcsh:Rmitochondrial haplogroupType 2 Diabetes Mellitusnutritional and metabolic diseasesGeneral Medicinemedicine.diseaseeye diseaseshumanities030104 developmental biologyEndocrinologychemistryglycemic controlnephropathybusinessHuman mitochondrial DNA haplogroup
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Branched-Chain Amino Acid Levels Are Related with Surrogates of Disturbed Lipid Metabolism among Older Men.

2016

Aims/hypothesis: Existing studies suggest that decreased branched-chain amino acid (BCAA) catabolism and thus elevated levels in blood are associated with metabolic disturbances. Based on such information, we have developed a hypothesis how BCAA degradation mechanistically connects to tricarboxylic acid cycle, intramyocellular lipid storage, and oxidation, thus allowing more efficient mitochondrial energy production from lipids as well as providing better metabolic health. We analyzed whether data from aged Finnish men are in line with our mechanistic hypothesis linking BCAA catabolism and metabolic disturbances. Methods: Older Finnish men enriched with individuals having been athletes in y…

0301 basic medicinemedicine.medical_specialtymitokondriotBranched-chain amino acideducationType 2 diabetesBiologyBody fat percentage03 medical and health scienceschemistry.chemical_compoundLipid oxidationlipid oxidationValineInternal medicineDiabetes mellitusenergy metabolismmedicinebranched-chain amino acidsta315Original Researchlcsh:R5-920Catabolismta3141General Medicinemedicine.diseasemetabolic disease3142 Public health care science environmental and occupational healthmitochondria030104 developmental biologyEndocrinologychemistry3121 General medicine internal medicine and other clinical medicinetricarboxylic acid cycleMedicineBlood sugar regulationlcsh:Medicine (General)Frontiers in Medicine
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