Search results for "fatty acid oxidation"

showing 6 items of 6 documents

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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Effects of insulin deficiency on exercise-induced acute responses in the regulation of fatty acid oxidation in mouse gastrocnemius muscles

2014

Insulin is a hormone that plays an important role in the regulation of the metabolism of all the main nutrients. Its main function is to stimulate glucose uptake and disposal or utilization by the cells and thus to decrease blood glucose concentration. However, it also inhibits breakdown of proteins and lipids and promotes their synthesis. Type 1 diabetes is a disease in which insulin secretion is impaired because of destruction of pancreatic β-cells. It is characterized by hyperglycemia and increased reliance on fat oxidation. This is seen also as altered gene expression patterns. The purpose of this study was to look into the effects of insulin deficiency on exercise-induced acute respons…

insulinexercisediabetesrasvahapothapettumineninsuliiniliikuntafatty acid oxidation
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Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via the DEPTOR-mTOR axis

2021

Objective Neddylation is a druggable and reversible ubiquitin-like post-translational modification upregulated in many diseases, including liver fibrosis, hepatocellular carcinoma, and more recently, non-alcoholic fatty liver disease (NAFLD). Herein, we propose to address the effects of neddylation inhibition and the underlying mechanisms in pre-clinical models of NAFLD. Methods Hepatic neddylation measured by immunohistochemical analysis and NEDD8 serum levels measured by ELISA assay were evaluated in NAFLD clinical and pre-clinical samples. The effects of neddylation inhibition by using a pharmacological small inhibitor, MLN4924, or molecular approaches were assessed in isolated mouse hep…

AdultMaleCoronavirus disease 2019 (COVID-19)AdolescentMLN4924[SDV.BC]Life Sciences [q-bio]/Cellular BiologyDiet High-Fat03 medical and health sciencesMiceYoung Adult0302 clinical medicineNon-alcoholic Fatty Liver DiseasePolitical scienceNAFLDmedia_common.cataloged_instanceAnimalsHumansEuropean unionNeddylationMolecular BiologyInternal medicineComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonAged0303 health sciencesTOR Serine-Threonine KinasesFatty AcidsIntracellular Signaling Peptides and ProteinsCell BiologyMiddle AgedRC31-12453. Good healthMice Inbred C57BLRare tumorDisease Models AnimalDeptor; Fatty acid oxidation; MLN4924; mTOR; NAFLD; NeddylationDeptorFatty acid oxidationHepatocytesmTOR030211 gastroenterology & hepatologyChristian ministryOriginal ArticleHumanitiesSignal Transduction
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Similar relative decline in aerobic and anaerobic power with age with in elite endurance and power master athletes of both sexes

2019

Lower physical activity levels in old age are thought to contribute to the age-related decline in peak aerobic and anaerobic power. Master athletes maintain high levels of physical activity with advancing age and endurance or power training may influence the extent to which these physical functions decline with advancing age. To investigate, 37-90-year-old power (n=20, 45% female) and endurance (n=19, 58% female) master athletes were recruited. Maximal aerobic power was assessed when cycling two-legged (VO2 Peak2-leg ) and cycling one-legged (VO2 Peak1-leg ), while peak jumping (anaerobic) power was assessed by a countermovement jump. Men and women had a similar VO2 Peak2-leg (mL·kg-1 ·min-…

AdultMalePhysical activityPhysical Therapy Sports Therapy and Rehabilitation030204 cardiovascular system & hematologymedicine.disease_cause03 medical and health sciences0302 clinical medicineAnimal scienceJumpingOxygen Consumptionmaster athletesFat oxidationmaksimaalinen hapenottoMedicineHumansOrthopedics and Sports MedicineMuscle Strengthta315fatty acid oxidationAgedAged 80 and overbiologyanaerobinen suorituskykybusiness.industryAthletesaging030229 sport sciencesta3142Middle Agedbiology.organism_classificationLipid MetabolismVO2PeakCross-Sectional StudiesikääntyminenAthletesPhysical FitnessageingPower ratioCountermovement jumpExercise TestPhysical EnduranceFemaleaerobinen suorituskykybusinessCyclingAnaerobic exerciseurheilijat
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A Dose-Dependent Improvement in Exercise Tolerance in Patients With Stable Angina Treated With Mildronate: A Clinical Trial “MILSS I”

2011

Objective. To assess the efficacy of various doses of Mildronate in combination with standard therapy for the exercise tolerance of patients with stable angina pectoris. The primary efficacy variable was the change in exercise time in bicycle ergometry from the baseline to 12 weeks of treatment. The secondary endpoints were the changes in maximum achieved load and time to the onset of angina from the baseline to week 12. Material and Methods. A total of 512 patients with chronic coronary heart disease who had ischemia as the limiting factor in the exercise test from 72 study centers in 4 countries were enrolled in this prospective, randomized, double-blind, placebo controlled phase 2 study.…

medicine.medical_specialtybusiness.industryIschemiaPhases of clinical researchGeneral Medicinemedicine.diseasePlaceboEffective dose (pharmacology)law.inventionSurgeryAnginaClinical trialDose–response relationshipmildronate; partial fatty acid oxidation inhibition; exercise tolerance; stable anginaRandomized controlled triallawAnesthesiamedicinebusinessMedicina; Volume 47; Issue 10; Pages: 78
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Substrate specificity overlap and interaction between Adrenoleukodystrophy protein (ALDP/ABCD1) and Adrenoleukodystrophy-related protein (ALDRP/ABCD2)

2011

X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disorder caused by mutations in the ABCD1 gene, which encodes a peroxisomal member of the ATP-binding cassette (ABC) transporter subfamily D called ALDP. ALDP is supposed to function as a homodimer allowing the entry of CoA-esters of very-long chain fatty acids (VLCFA) into the peroxisome, the unique site of their β-oxidation. ALDP deficiency can be corrected by overexpression of ALDRP, its closest homolog. However, the exact nature of the substrates transported by ALDRP and its relationships with ALDP still remain unclear. To gain insight into the function of ALDRP, we used cell models allowing the induction in a dose-dependent m…

congenital hereditary and neonatal diseases and abnormalitiesendocrine system diseasesATP-binding cassette transportermembrane proteinsBiologyATP Binding Cassette Transporter Subfamily DBiochemistry03 medical and health sciences0302 clinical medicineabc transporterCell Line TumormedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Molecular BiologyBeta oxidationfatty acid oxidation030304 developmental biologychemistry.chemical_classification0303 health sciencesadrenoleukodystrophyabc transporter;fatty acid;fatty acid oxidation;membrane proteins;peroxisomes;adrenoleukodystrophyFatty AcidsNeurosciencesWild typeFatty acidnutritional and metabolic diseasesperoxisomesCell BiologyPeroxisomemedicine.diseaseLipidsRatschemistryMembrane proteinBiochemistry[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurons and CognitionATP-Binding Cassette TransportersAdrenoleukodystrophy[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]fatty acidOxidation-Reduction030217 neurology & neurosurgeryPolyunsaturated fatty acid
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