grant
Uncovering the mechanistic drivers of hepatic dysfunction in LIPT1 deficiency
Organization UT SOUTHWESTERN MEDICAL CENTERLocation DALLAS, UNITED STATESPosted 1 May 2025Deadline 30 Apr 2029
NIHUS FederalResearch GrantFY20250-11 years old1,2-Dithiolane-3-pentanoic acid2-Keto-4-Hydroxyglutarate Dehydrogenase2-Oxoglutarate Dehydrogenase2-Oxoglutarate Dehydrogenase ComplexAcetatesAcetyl CoAAcetyl Coenzyme AAcuteAgeAmino AcidsAmpullary CrestAttenuatedAutomobile DrivingAutoregulationBasic ResearchBasic ScienceBody Weight decreasedBypassCarbamideCarbonCategoriesCessation of lifeChildChild YouthChildren (0-21)ChronicCirculationCitric Acid CycleClinicalClinical Medical SciencesClinical MedicineComplexCrista ampullarisCytolysisD-GlucoseDNA mutationDataDeathDefectDehydrogenasesDevelopmentDextroseDietDietary InterventionDietary SupplementationDiseaseDisorderDysfunctionEarly InterventionEarly identificationElaqua XXElectron MicroscopyEnzyme GeneEnzymesFDA approvedFatty AcidsFunctional disorderGeneralized GrowthGenetic ChangeGenetic DiseasesGenetic defectGenetic mutationGenus HippocampusGlnGlucoseGlutamineGrowthGrowth and DevelopmentGrowth and Development functionHealthHepaticHepatic DisorderHepatic GlycogenHepatic mitochondriaHepatotoxic effectHepatotoxicityHereditary Metabolic DisorderHomeostasisHospital AdmissionHospitalizationHumulin RHypoglycemiaImpairmentInborn Errors of MetabolismIncidenceIndividualInfant MortalityInfant Mortality TotalInjury to LiverInsulinIntermediary MetabolismInterventionKO miceKeto AcidsKetoglutarate Dehydrogenase ComplexKnock-outKnock-out MiceKnockoutKnockout MiceKrebs CycleL-GlutamineLactic AcidosisLipidsLipoic AcidLiverLiver GlycogenLiver MitochondriaLiver ToxicityLiver diseasesLysisMaintenanceMeasuresMetabolicMetabolic DiseasesMetabolic DisorderMetabolic ProcessesMetabolic dysfunctionMetabolismMiceMice MammalsMitochondriaModelingMorphologyMurineMusMutationNeurodevelopmental DisabilityNovolin RNucleotidesNull MouseNutrientNutrition InterventionsNutritional InterventionsOralOxidoreductaseOxidoreductase GeneOxoglutarate DehydrogenasePathologicPathologyPatientsPhysiological HomeostasisPhysiologyPhysiopathologyPost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingProtein ModificationProteinsPyruvatePyruvate CarboxylaseQ LevoglutamideQ. LevoglutamideReductasesRegular InsulinRegulationResearchRespirationRoleS-acetate Coenzyme ASeahorseStable Isotope LabelingStructureSystemic diseaseTCA cycleTestingTherapeuticTherapeutic InterventionTherapeutic UsesThesaurismosisThioctic AcidTimeTissue GrowthToxic effect on liver cellsTricarboxylic Acid CycleUreaUrea CarbamideUreaphilWeight LossWeight ReductionWorkagesalpha-Ketoglutarate Dehydrogenasealpha-Ketoglutarate Dehydrogenase Complexalpha-Lipoic Acidaminoacidattenuateattenuatesbody weight losscarboxylationcareercrista ampullacristaedeath among infantsdeath in first year of lifedeath in infancydeath in infantsdevelopmentaldiet interventiondiet supplementationdietsdrivingearly childhoodfatty acid oxidationflexibilityflexiblegenetic conditiongenetic disordergenome mutationhepatic body systemhepatic damagehepatic diseasehepatic injuryhepatic metabolismhepatic organ systemhepatic toxicityhepatocyte injuryhepatopathyhepatoxicityhypoglycemichypoglycemic episodesimprovedin vivoinborn metabolism disorderinfant deathinfant demiseinfantile deathintervention therapyketoacidketogenicketogentickidsliver damageliver disorderliver injuryliver metabolismlong chain fatty acidmetabolism disordermetabolism measurementmetabolomicsmetabonomicsmitochondrialmortality in infantsmouse modelmurine modelnovelontogenyorganic acidoxidationpathophysiologypreventpreventingpyruvate dehydrogenasepyruvic carboxylaserare genetic diseaserare genetic disorderrespiratory mechanismskillssocial rolestable isotopestressorsuccinyl-CoAsuccinyl-coenzyme Aurea cyclewt-lossyoungster
Description preview
PROJECT SUMMARY/ABSTRACT
Inborn errors of metabolism (IEMs) are genetic diseases that often cause severe illness and death in infancy or
early childhood. IEMs represent the largest subset of genetic diseases in children, numbering over 1000, with a
combined incidence greater than 1 in 1000. For some IEMs, early identification and intervention…
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