grant
Beta cell adaptation mechanisms during caloric restriction and ER stress
Organization VANDERBILT UNIVERSITYLocation Nashville, UNITED STATESPosted 1 Jan 2024Deadline 31 Dec 2028
NIHUS FederalResearch GrantFY202521+ years old3-D3-Dimensional3DAdultAdult HumanAdult-Onset Diabetes MellitusAffectAgingAutoregulationBasal Transcription FactorBasal transcription factor genesBeta CellBlood GlucoseBlood SugarCaloric RestrictionCell AgingCell BodyCell ComponentsCell FunctionCell MaturationCell PhysiologyCell ProcessCell SenescenceCell StructureCellsCellular AgingCellular FunctionCellular PhysiologyCellular ProcessCellular SenescenceCellular StressCellular Stress ResponseCellular StructuresCharacteristicsChromatinChronicD-GlucoseDNA DamageDNA InjuryDataDevelopmentDextroseDiabetes MellitusDiabetic mouseDietDiet CompositionDiseaseDisorderDysfunctionER stressEconomic BurdenElectronsEndocrine Gland SecretionEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessExposure toFaceFunctional disorderGene InactivationGene SilencingGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGenetic TranscriptionGenomeGenomicsGlucoseGoalsHealthHeterogeneityHigh Fat DietHistonesHomeostasisHormonesHumanHumulin RImmunocompromisedImmunocompromised HostImmunocompromised PatientImmunosuppressed HostImpairmentIn SituIn VitroIndividualInsulinInsulin CellInsulin Secreting CellIslands of Langerhans TransplantationIslands of Pancreas TransplantationIslet CellIslets of Langerhans GraftingIslets of Langerhans TransplantationIsotopesKetosis-Resistant Diabetes MellitusL-LysineLabelLength of LifeLightLongevityLysineMapsMass Photometry/Spectrum AnalysisMass SpectrometryMass SpectroscopyMass SpectrumMass Spectrum AnalysesMass Spectrum AnalysisMaturity-Onset Diabetes MellitusMetabolicMethylationMiceMice MammalsMicroscopyMitochondriaModern ManMolecularMurineMusNIDDMNegative Beta ParticleNegatronsNitrogenNon-Insulin Dependent DiabetesNon-Insulin-Dependent Diabetes MellitusNoninsulin Dependent DiabetesNoninsulin Dependent Diabetes MellitusNormalcyNormalitiesNovolin RPancreatic Islets TransplantationPancreatic beta CellPancreatic β-CellPathway interactionsPatientsPatternPeripheralPhotoradiationPhysiologicPhysiologicalPhysiological HomeostasisPhysiopathologyPopulationPrediabetesPrediabetes syndromePrediabetic StateProcessProductionProliferatingPropertyProteinsRNA ExpressionRegular InsulinReplicative SenescenceResolutionSense OrgansSlow-Onset Diabetes MellitusStable Diabetes MellitusStressStructure of beta Cell of isletSubcellular ProcessT2 DMT2DT2DMTechniquesTherapeutic HormoneTranscriptionTranscription Factor Proto-OncogeneTranscription factor genesType 2 Diabetes MellitusType 2 diabetesType II Diabetes MellitusType II diabetesUpregulationWorkadult onset diabetesadulthoodage associatedage correlatedage dependentage linkedage relatedage specificautologous islet transplantationblood glucose regulationbuild resiliencebuild resiliencycalorie restrictioncell stresscircadian regulationcompare to controlcomparison controldevelop resiliencedevelop resiliencydevelopmentaldiabetesdiabetes mouse modeldiabeticdiet controldietary compositiondietary controldietingdietsendoplasmic reticulum stressenhance resilienceenhance resiliencyepigenetic profilingepigeneticallyepigenomeexpectationexperienceexperimentexperimental researchexperimental studyexperimentsfacesfacialfacilitate resiliencegene locusgenetic locusgenomic locationgenomic locusglucose controlglucose homeostasisglucose regulationhallmarks of aginghistone modificationimaging spectroscopyimmunosuppressed patientimprove resilienceimprove resiliencyimprovedin vivoincrease resilienceincrease resiliencyinsightinsulin secretioninsulin sensitivityisletislet auto transplantationislet beta cell transplantationislet cell transplantislet cell transplantationislet transplantationketosis resistant diabetesmaturity onset diabetesmetabolic phenotypemetabotypemitochondrialmultiomicsmultiple omicsnormalityold agepancreas beta cellpancreas β cellpancreatic b-cellpanomicspathophysiologypathwaypillars of agingpostmitoticpre-diabetespre-diabeticprediabeticpreservationpreventpreventingpromote resiliencepromote resiliencyprotein homeostasisproteostasisreplicative agingresilience developmentresolutionsresponsesocialspectroscopic imagingstable isotopethree dimensionaltooltranscription factortranscriptional silencingtranscriptomicstransplant modeltype 2 DMtype II DMtype two diabetesβ-cellβ-cellsβCell
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Project Summary
Type 2 diabetes (T2D) is caused by the collapse of glucose homeostasis mechanisms, and the odds of devel-
oping T2D increase during old age. Beta cells make insulin, a major hormone involved in the regulation of glucose
homeostasis; these cells modulate insulin release in response to changes in blood glucose levels and/or meta-…
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