Search results for "PGC"

showing 10 items of 26 documents

Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
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Moderate exercise in mice improves cancer plus chemotherapy-induced muscle wasting and mitochondrial alterations

2019

Cancer cachexia is a multifactorial syndrome characterized by anorexia, body wasting, and muscle and adipose tissue loss, impairing patient's tolerance to anticancer treatments and survival. The aim of the present study was to compare the effects induced in mice by tumor growth alone (C26) or in combination with chemotherapy [C26 oxaliplatin and 5-fluorouracil (oxfu)] and to evaluate the potential of moderate exercise. Oxfu administration to C26 mice exacerbated muscle wasting and triggered autophagy or mitophagy, decreased protein synthesis, and induced mitochondrial alterations. Exercise in C26 oxfu mice counteracted the loss of muscle mass and strength, partially rescuing autophagy and m…

0301 basic medicineMaleCachexiamedicine.medical_treatmentPGC-1αMitochondrionliikuntaBiochemistryMice0302 clinical medicineNeoplasmsMitophagyautophagy; cancer cachexia; mitochondria; PGC-1α; survival; Biotechnology; Biochemistry; Molecular Biology; Geneticsta315WastingMice Inbred BALB C3. Good healthmitochondriaMuscular AtrophyFemalemedicine.symptomBiotechnologycancer cachexiamedicine.medical_specialtyautophagyAntineoplastic AgentsAnorexiasurvivalCachexia03 medical and health sciencesInternal medicinePhysical Conditioning AnimalGeneticsmedicineAnimalsMuscle SkeletalMolecular BiologyChemotherapysyöpähoidotbusiness.industryAutophagyCancermedicine.diseaseta3122030104 developmental biologyEndocrinologyQuality of Lifekoe-eläinmallitbusinessEnergy Metabolismlihassurkastumasairaudet030217 neurology & neurosurgeryFASEB Journal
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Skeletal muscle Heat shock protein 60 increases after endurance training and induces peroxisome proliferator-activated receptor gamma coactivator 1 α…

2016

AbstractHeat shock protein 60 (Hsp60) is a chaperone localizing in skeletal muscle mitochondria, whose role is poorly understood. In the present study, the levels of Hsp60 in fibres of the entire posterior group of hindlimb muscles (gastrocnemius, soleus and plantaris) were evaluated in mice after completing a 6-week endurance training program. The correlation between Hsp60 levels and the expression of four isoforms of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) were investigated only in soleus. Short-term overexpression of hsp60, achieved by in vitro plasmid transfection, was then performed to determine whether this chaperone could have a role in the activa…

0301 basic medicineMaleTime FactorsPPARgammaPeroxisome proliferator-activated receptorExosomesMiceendurance trainingMyocytechemistry.chemical_classificationMultidisciplinarytrainingbiologyHsp60Mitochondriamedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle Fibers Fast-TwitchHsp60; skeletal muscle; training; PPARgamma; PGC1αHSP60[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Oxidation-Reductionmedicine.medical_specialtyanimal structureschemical and pharmacologic phenomenacomplex mixturescachexiaArticleCell Line03 medical and health sciencesEndurance trainingHeat shock proteinInternal medicinePhysical Conditioning AnimalPGC1αCoactivatormedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]skeletal muscleMuscle SkeletalSettore BIO/16 - Anatomia UmanafungiSkeletal muscleChaperonin 60030104 developmental biologyEndocrinologychemistryGene Expression RegulationChaperone (protein)biology.proteinPhysical EnduranceBiomarkersTranscription FactorsScientific Reports
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Peroxisome proliferator-activated receptor-γ coactivator-1α mediates neuroprotection against excitotoxic brain injury in transgenic mice: role of mit…

2016

Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcriptional coactivator involved in the regulation of mitochondrial biogenesis and cell defense. The functions of PGC-1α in physiology of brain mitochondria are, however, not fully understood. To address this we have studied wild-type and transgenic mice with a two-fold overexpression of PGC-1α in brain neurons. Data showed that the relative number and basal respiration of brain mitochondria were increased in PGC-1α transgenic mice compared with wild-type mitochondria. These changes occurred concomitantly with altered levels of proteins involved in oxidative phosphorylation (OXPHOS) as studied by proteomi…

0301 basic medicineProgrammed cell deathKainic acidTransgenebcl-X ProteinPeroxisome proliferator-activated receptorBiologyInhibitor of apoptosisSettore BIO/09 - FisiologiaNeuroprotectionOxidative PhosphorylationInhibitor of Apoptosis ProteinsMice03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineBrain InjurieInhibitor of Apoptosis ProteinAnimalsCA1 Region HippocampalCells CulturedNeuronschemistry.chemical_classificationNeuroscience (all)Kainic AcidCell DeathAnimalNeuron survivalGeneral NeuroscienceProteomicXIAP; Kainic acid; Mitochondria; Neuron survival; PGC-1α; Proteomics; Animals; Brain Injuries; CA1 Region Hippocampal; Cell Death; Cells Cultured; Inhibitor of Apoptosis Proteins; Kainic Acid; Mice; Mitochondria; Neurons; Oxidative Phosphorylation; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Neuroscience (all)NeuronPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyXIAP030104 developmental biologyProto-Oncogene Proteins c-bcl-2chemistryMitochondrial biogenesisBrain InjuriesImmunologyPGC-1α030217 neurology & neurosurgeryEuropean Journal of Neuroscience
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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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Molecular basis of the effects of argan oil on mitochondrial and peroxisomal metabolism of the fatty acids and inflammation

2012

The objective of this thesis work was to explore the molecular basis of Argan Oil (AO) effects on the mitochondrial and peroxisomal lipid metabolism and to elucidate its anti-inflammatory potential. We thus showed, initially, that the artisanal method preparation preserved the antioxidant properties of AO preventing the oxidation of the ferulic acid, by contrast to AO of commercial origin. Then, the treatment by the AO or lipopolysaccharides (LPS) of human fibroblasts, the cellular model of pseudo-neonatal adrenoleukodystrophy (P-NALD), revealed for the AO that peroxisomes proliferation is independent from the activation of the nuclear receptor PPARα and the co-activator PGC-1α. On the othe…

Acide féruliqueLPSACADsPGC-1αArganPPARαTNFα[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciencesInflammation[SDV.SA] Life Sciences [q-bio]/Agricultural sciencesIL-6GluconeogenesisP-NALDFerulic acidMitochondrieLipid MetabolismFatty acidMétabolisme lipidiqueAntioxydantMitochondriaAcide grasLiverΒ-oxidationNéoglucogenèseAntioxidantACOX1PeroxysomeFoieIL10Β-oxydation
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Exercise and antioxidant supplements in the elderly

2013

Abstract Both exercise and aging increase reactive oxygen species (ROS), which can result in damage to cells. Aging is the result of damage caused by ROS to the mitochondrial genome in post mitotic cells and numerous studies have demonstrated an increase in ROS or their byproducts with exercise. ROS can cause oxidative stress as they overwhelm the antioxidant cellular defenses. Therefore interventions aimed at limiting or inhibiting ROS production, such as supplementation with antioxidant vitamins, should be able to reduce fatigue during muscle contraction and the rate of formation of aging changes with a consequent reduction of the aging rate and disease pathogenesis. However, it has been …

Cell signalingAgingAntioxidantmedicine.medical_treatmentmedia_common.quotation_subjectPopulationPGC-1αSkeletal musclePhysical Therapy Sports Therapy and RehabilitationPharmacologyBiologymedicine.disease_causeNF-κBchemistry.chemical_compoundmedicineOrthopedics and Sports Medicineeducationmedia_commonchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesAdaptationsLongevitySkeletal muscleNF-κBmedicine.anatomical_structurechemistryBiochemistryOxidative stressAntioxidant enzymesOxidative stressJournal of Sport and Health Science
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Fibroblast Growth Factor-21 (FGF-21) enhances mitochondrial functions and increases the activity of PGC-1α in human dopaminergic neurons.

2014

FGF-21 è un fattore di crescita ad azione endocrina principalmente espresso nel fegato con funzioni metaboliche; induce a livello epatico e in altri tessuti incremento di PGC1, ma le sue funzioni a livello cerebrale sono ancora sconosciute. PGC1 è espresso anche nel cervello dove mostra azione neuroprotettiva in neuroni dopaminergici in modelli animali di morbo di Parkinson. Scopo della ricerca era indagare possibili correlazioni tra le due proteine a livello cerebrale. I dati mostrano che FGF-21 induce attivazione di PGC1 mediante la deacetilasi Sirtuina-1 NAD+ dipendente, in neuroni dopaminergici e un incremento dell’attività respiratoria mitocondriale. FGF-21 risulta espresso nel cerv…

FGF-21parkinson diseaseSettore BIO/09 - FisiologiaPGC-1alpha
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Fibroblast growth factor-21 enhances mitochondrial functions and increases the activity of PGC-1α in human dopaminergic neurons via Sirtuin-1

2014

Abstract Mitochondrial dysfunctions accompany several neurodegenerative disorders and contribute to disease pathogenesis among others in Parkinson’s disease (PD). Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) is a major regulator of mitochondrial functions and biogenesis, and was suggested as a therapeutic target in PD. PGC-1α is regulated by both transcriptional and posttranslational events involving also the action of growth factors. Fibroblast growth factor-21 (FGF21) is a regulator of glucose and fatty acid metabolism in the body but little is known about its action in the brain. We show here that FGF21 increased the levels and activity of PGC-1α and elevated mito…

FGF21educationRegulatorNicotinamide phosphoribosyltransferasePGC-1αFGF21; PGC-1α; SIRT1; Dopaminergic neurons; Mitochondria; Parkinson’s diseaseMitochondrionBioinformaticsDopaminergic neuronsSettore BIO/09 - Fisiologia03 medical and health scienceschemistry.chemical_compoundFGF21SIRT10302 clinical medicineDopaminergic Cell030304 developmental biologyDopaminergic neuron0303 health sciencesMultidisciplinarybiologySirtuin 1ResearchDopaminergicMitochondriaCell biologychemistryParkinson’s diseasebiology.protein3111 BiomedicineNAD+ kinase030217 neurology & neurosurgerySpringerPlus
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