Search results for "MESH: Mitochondria"

showing 10 items of 10 documents

Effects of a high-fat diet on energy metabolism and ROS production in rat liver.

2011

International audience; BACKGROUND & AIMS: A high-fat diet affects liver metabolism, leading to steatosis, a complex disorder related to insulin resistance and mitochondrial alterations. Steatosis is still poorly understood since diverse effects have been reported, depending on the different experimental models used. METHODS: We hereby report the effects of an 8 week high-fat diet on liver energy metabolism in a rat model, investigated in both isolated mitochondria and hepatocytes. RESULTS: Liver mass was unchanged but lipid content and composition were markedly affected. State-3 mitochondrial oxidative phosphorylation was inhibited, contrasting with unaffected cytochrome content. Oxidative…

Mitochondrial ROSMaleTranscription GeneticMESH : Reactive Oxygen SpeciesMitochondria LiverMESH : HepatocytesMitochondrionOxidative PhosphorylationMESH: Hepatocytes0302 clinical medicineMESH: Membrane Potential MitochondrialCitrate synthaseMESH: AnimalsBeta oxidationMESH : Electron Transport2. Zero hungerMembrane Potential Mitochondrial0303 health sciencesMESH : RatsAdenine nucleotide translocatorMESH: Energy MetabolismMESH: Reactive Oxygen SpeciesLipidsBiochemistryLiverMESH: Dietary FatsMitochondrial matrix030220 oncology & carcinogenesisBody CompositionMESH : Oxidative PhosphorylationATP–ADP translocaseMESH: Mitochondria LiverMESH: RatsMESH : Body CompositionMESH : MaleOxidative phosphorylationBiologyMESH : Rats WistarElectron Transport03 medical and health sciencesMESH: Oxidative Phosphorylation[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats WistarMESH: Electron Transport[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyHepatologyMESH: Transcription GeneticMESH : Transcription GeneticMESH : LiverMESH : LipidsMESH: Body CompositionMESH: Rats WistarMESH: LipidsDietary FatsMESH: MaleRatsMESH : Energy MetabolismMESH : Membrane Potential MitochondrialMESH : Mitochondria Liverbiology.proteinHepatocytesMESH : AnimalsEnergy MetabolismReactive Oxygen SpeciesMESH : Dietary FatsMESH: Liver
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Immunoaffinity purification and characterization of mitochondrial membrane-bound D-3-hydroxybutyrate dehydrogenase from Jaculus orientalis.

2008

Abstract Background The interconversion of two important energy metabolites, 3-hydroxybutyrate and acetoacetate (the major ketone bodies), is catalyzed by D-3-hydroxybutyrate dehydrogenase (BDH1: EC 1.1.1.30), a NAD+-dependent enzyme. The eukaryotic enzyme is bound to the mitochondrial inner membrane and harbors a unique lecithin-dependent activity. Here, we report an advanced purification method of the mammalian BDH applied to the liver enzyme from jerboa (Jaculus orientalis), a hibernating rodent adapted to extreme diet and environmental conditions. Results Purifying BDH from jerboa liver overcomes its low specific activity in mitochondria for further biochemical characterization of the e…

lcsh:Animal biochemistryMESH : AgedMESH : RodentiaMESH: RodentiaMESH: Base SequenceBiochemistryMESH: Lipid PeroxidationMESH : Information ServicesAntigen-Antibody ReactionsMESH: Health EducationEpitopesMESH: OrganizationsMESH: LibrariesMESH: Antigen-Antibody Reactionslcsh:QD415-436MESH: AnimalsMESH : OrganizationsMESH : Physician's RoleMESH: Bacterial ProteinsImmunosorbent Techniqueschemistry.chemical_classificationMESH: Conserved SequenceMethodology ArticleMESH : Computer Communication NetworksMESH: Chromatography AffinityMESH : Pseudomonas aeruginosaMESH : Chromatography AffinityMESH : Immunosorbent TechniquesMESH: Ethnic GroupsMESH : Ethnic GroupsMESH: EpitopesMESH : Patient SatisfactionMESH : United StatesMESH: MitochondriaMESH : Antigen-Antibody ReactionsMolecular Sequence DataMESH : Hydroxybutyrate DehydrogenaseMESH: Sequence AlignmentRodentiaMESH: Information ServicesMESH : Epitopeslcsh:BiochemistryMESH : Mitochondrial MembranesBacterial ProteinsMESH : Conserved SequenceComplementary DNAMESH : LibrariesMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Immunosorbent TechniquesMESH: Molecular Sequence DataMESH: HumansMESH : Consumer ParticipationMESH : HumansMESH: AdultMESH: Patient SatisfactionMESH: Hydroxybutyrate DehydrogenaseMESH: Consumer ParticipationchemistryLipid PeroxidationMESH: FemaleMESH: LiverMESH : Sequence Analysis DNAMESH: Continental Population GroupsMESH: Sequence Analysis DNAMESH : Molecular Sequence DataDehydrogenaseChromatography AffinityMESH: Mitochondrial MembranesMESH: Antibodies BacterialMESH : Bacterial ProteinsMESH : FemaleMESH: Computer Communication NetworksConserved SequenceMESH: AgedbiologyMESH : Lipid PeroxidationMESH : Sequence AlignmentMESH: Physician's RoleMESH : AdultAntibodies BacterialMitochondriaAmino acidLiverBiochemistryMitochondrial MembranesPseudomonas aeruginosaMESH: Pseudomonas aeruginosaMESH : MitochondriaMESH : Mass MediaMESH: Mass MediaMESH : MaleHydroxybutyrate DehydrogenaseAffinity chromatographyMESH : Health Education[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: United StatesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Antibodies Bacteriallcsh:QP501-801Jaculus orientalisMESH : Continental Population GroupsBase SequenceMESH : LiverSequence Analysis DNAbiology.organism_classificationMolecular biologyMESH: MaleEnzymePolyclonal antibodiesbiology.proteinMESH : Base SequenceNAD+ kinaseMESH : AnimalsSequence Alignment
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Abnormalities of mitochondrial functioning can partly explain the metabolic disorders encountered in sarcopenic gastrocnemius.

2007

International audience; Aging triggers several abnormalities in muscle glycolytic fibers including increased proteolysis, reactive oxygen species (ROS) production and apoptosis. Since the mitochondria are the main site of substrate oxidation, ROS production and programmed cell death, we tried to know whether the cellular disorders encountered in sarcopenia are due to abnormal mitochondrial functioning. Gastrocnemius mitochondria were extracted from adult (6 months) and aged (21 months) male Wistar rats. Respiration parameters, opening of the permeability transition pore and ROS production, with either glutamate (amino acid metabolism) or pyruvate (glucose metabolism) as a respiration substr…

Malemuscle atrophyMESH : Cell Aging[SDV]Life Sciences [q-bio]MESH : Reactive Oxygen SpeciesMitochondrion0302 clinical medicineGlycolysisMESH: AnimalsMESH : Muscle SkeletalMESH : Fatty AcidsCellular SenescencePhospholipidsMESH: Superoxide Dismutasereactive oxygen speciesMESH : Free Radicals0303 health sciencesMESH: Muscle SkeletalMESH : RatsFatty Acidsfatty acid profile of mitochondrial lipidsMESH: Reactive Oxygen SpeciesPyruvate dehydrogenase complexMESH: Fatty Acidsmitochondria[SDV] Life Sciences [q-bio]BiochemistryMESH: Cell AgingMESH: CalciumMESH : MitochondriaCell agingPyruvate decarboxylationmedicine.medical_specialtyFree RadicalsMESH: RatsCellular respirationMESH: MitochondriaMESH : MaleCell Respirationchemistry.chemical_elementOxidative phosphorylationBiologyCalciumMESH : Rats WistarMESH : Phospholipids03 medical and health sciencesMESH: Free RadicalsInternal medicinemedicineAnimalsMESH : Superoxide DismutaseRats WistarMuscle SkeletalMESH : Calcium030304 developmental biologyMESH: Phospholipidscalciumpermeability transition poreSuperoxide Dismutaseagingaging;calcium;fatty acid profile of mitochondrial lipids;mitochondria;muscle atrophy;permeability transition pore;reactive oxygen species;Animals;Calcium;Cell Aging;Cell Respiration;Fatty Acids;Free Radicals;Male;Mitochondria;Muscle;Skeletal;Phospholipids;Rats;Wistar;Reactive Oxygen Species;Superoxide DismutaseCell BiologyMESH: Rats WistarMESH: MaleRatsEndocrinologychemistryMESH : Cell RespirationMESH : AnimalsMESH: Cell Respiration030217 neurology & neurosurgery
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells.

2011

SUMMARYAlthough many cancer cells are primed for apoptosis, they usually develop resistance to cell death at multiple levels. Permeabilization of the outer mitochondrial membrane, which is mediated by proapoptotic Bcl-2 family members like Bax, is considered as a point-of-no-return for initiating apoptotic cell death. This crucial role has placed Bcl-2 family proteins as recurrent targets for anticancer drug development. Here, we propose and demonstrate a new concept based on using minimal active version of Bax to induce cell death independently of endogenous Bcl-2 proteins. We show that membrane-active segments of Bax can directly induce the release of mitochondria-residing apoptogenic fac…

ApoptosisMitochondrionMiceMESH: Protein Structure Tertiary0302 clinical medicineNeoplasmsgeneticsMESH: AnimalsMESH: Neoplasmsbcl-2-Associated X Protein0303 health sciencesbiologyMESH: PeptidesCytochrome capoptosisCytochromes cMESH: Cytochromes cproapoptotic BaxCell biologyMitochondriadrug therapymitochondria030220 oncology & carcinogenesisBacterial outer membraneProgrammed cell deathMESH: Cell Line TumorMESH: MitochondriaAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancerpore-forming peptideschemistryArticle03 medical and health sciencesBcl-2-associated X proteinBcl-2 familyCell Line TumorAnimalsHumansMESH: bcl-2-Associated X ProteinMESH: Mice030304 developmental biologyMESH: HumansMESH: ApoptosisBcl-2 familyCell BiologyProtein Structure Tertiaryanticancer agentantivascular therapyApoptosisdrug effectsCancer cellbiology.proteinMESH: Antineoplastic AgentspharmacologyphysiopathologyPeptidesmetabolism
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Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.

2012

Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice…

MESH: Oxidation-Reduction[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEndocrinology Diabetes and MetabolismGlucose uptakeAMP-Activated Protein KinasesInbred C57BLMice0302 clinical medicineAMP-activated protein kinaseMESH : Lipid MetabolismHyperinsulinemiaMESH: AnimalsMESH: AMP-Activated Protein KinasesMESH : Muscle SkeletalMESH : Fatty AcidsBeta oxidationMESH: Lipid Metabolism0303 health sciencesMESH: Muscle SkeletalbiologyMESH : Diet High-FatFatty AcidsMESH: Energy MetabolismMESH : AMP-Activated Protein KinasesMESH: Mitochondria MuscleSkeletal3. Good healthApelinMitochondriaMESH: Fatty AcidsMESH : Cyclic AMP-Dependent Protein KinasesMESH: Insulin ResistanceAlimentation et NutritionApelinIntercellular Signaling Peptides and ProteinsMuscleMESH : Insulin ResistanceOxidation-Reductionmedicine.medical_specialtyMESH : Mitochondria Muscle030209 endocrinology & metabolismMESH : Mice Inbred C57BLMESH: Cyclic AMP-Dependent Protein KinasesDiet High-Fat03 medical and health sciencesInsulin resistanceAdipokinesMESH: Mice Inbred C57BLInternal medicineMESH : MiceInternal MedicinemedicineFood and NutritionAnimalsMuscle SkeletalMESH: Intercellular Signaling Peptides and ProteinsMESH: MiceMESH : Intercellular Signaling Peptides and Proteins030304 developmental biologyMESH : Oxidation-ReductionAMPKmedicine.diseaseLipid MetabolismCyclic AMP-Dependent Protein KinasesMitochondria MuscleDietMice Inbred C57BLMESH : Energy Metabolism[SDV.AEN] Life Sciences [q-bio]/Food and NutritionAMP-Activated Protein Kinases;Animals;Cyclic AMP-Dependent Protein Kinases;Diet;High-Fat;Energy Metabolism;Fatty Acids;Insulin Resistance;Intercellular Signaling Peptides and Proteins;Lipid Metabolism;Mice;Inbred C57BL;Mitochondria;Muscle;Skeletal;Oxidation-ReductionHigh-FatMESH: Diet High-FatMetabolismEndocrinologyMitochondrial biogenesisbiology.proteinMESH : AnimalsInsulin ResistanceEnergy Metabolism[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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FRET multiphoton spectral imaging microscopy of 7-ketocholesterol and Nile Red in U937 monocytic cells loaded with 7-ketocholesterol.

2004

To show the effect of 7-ketocholesterol (7KC) on cellular lipid content by means of flow cytometry and the interaction of 7KC with Nile Red (NR) via ultraviolet fluorescence resonance energy transfer (FRET) excitation of NR on U937 monocytic cells by means of 2-photon excitation confocal laser scanning microscopy (CLSM).Untreated and 7KC-treated U937 cells were stained with NR and analyzed by flow cytometry and CLSM. 3D sequences of images were obtained by spectral analysis in a 2-photon excitation CLSM and analyzed by the factor analysis of medical image sequences (FAMIS) algorithm, which provides factor curves and images. Factor images are the result of the FAMIS image processing method, …

MESH: Cell DeathMESH: Fluorescence Resonance Energy TransferMESH: Mitochondria[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/ImagingMESH : Flow CytometryMESH: Flow CytometryMESH: U937 CellsMESH: MonocytesMonocytesMembrane PotentialsMESH : Staining and LabelingMESH : Microscopy Fluorescence MultiphotonOxazinesFluorescence Resonance Energy TransferImage Processing Computer-AssistedHumansMESH: Membrane PotentialsMESH: Microscopy ConfocalMESH : Membrane PotentialsMESH : Fluorescent DyesMESH : Microscopy ConfocalKetocholesterols[ SDV.IB.IMA ] Life Sciences [q-bio]/Bioengineering/ImagingFluorescent DyesMESH : KetocholesterolsMicroscopy ConfocalMESH: HumansMESH : OxazinesCell DeathStaining and LabelingMESH : HumansMESH: KetocholesterolsU937 CellsFlow CytometryMESH: Fluorescent DyesMESH: Image Processing Computer-AssistedMitochondriaMESH: Staining and Labeling[SDV.IB.IMA] Life Sciences [q-bio]/Bioengineering/ImagingMicroscopy Fluorescence MultiphotonMESH : MonocytesMESH : Fluorescence Resonance Energy TransferMESH : Cell DeathMESH : U937 CellsMESH: Microscopy Fluorescence MultiphotonMESH : MitochondriaMESH: OxazinesMESH : Image Processing Computer-Assisted
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Prehibernation and hibernation effects on the D-3-hydroxybutyrate dehydrogenase of the heavy and light mitochondria from liver jerboa (Jaculus orient…

2007

The D-3-hydroxybutyrate dehydrogenase (BDH) (EC 1.1.1.30) from liver jerboa (Jaculus orientalis), a ketone body converting enzyme in mitochondria, in two populations of mitochondria (heavy and light) has been studied in different jerboa states (euthermic, prehibernating and hibernating). The results reveal: (1) important variations between states in terms of ketones bodies, glucose and lipid levels; (2) significant differences between the BDH of the two mitochondrial populations in term of protein expression and kinetic properties. These results suggest that BDH leads an important conformational change depending on the physiological state of jerboa. This BDH structural change could be the c…

HibernationMESH: RatsMESH : HibernationMESH : Hydroxybutyrate DehydrogenaseMESH : RodentiaMESH: RodentiaFluorescent Antibody TechniqueMitochondria LiverRodentiaDehydrogenaseMitochondrionBiochemistryMESH : PhospholipidsHydroxybutyrate DehydrogenaseHibernation[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsMESH: Animals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyInner mitochondrial membraneMESH: Fluorescent Antibody TechniqueJaculus orientalis[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPhospholipidsMESH: Phospholipidschemistry.chemical_classificationMESH: KineticsbiologyMESH : RatsGeneral MedicineMetabolismbiology.organism_classificationRatsMESH: Hydroxybutyrate DehydrogenaseKineticsMESH : Fluorescent Antibody TechniqueEnzymechemistryBiochemistryMESH : Mitochondria LiverKetone bodiesMESH: Hibernationsense organsMESH : AnimalsMESH : KineticsMESH: Mitochondria Liver
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