grant
The role of B cell estrogen signaling in menopause-associated metabolic dysfunction
Organization UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTRLocation OKLAHOMA CITY, UNITED STATESPosted 1 Feb 2019Deadline 31 May 2030
NIHUS FederalResearch GrantFY2025AbdomenAdipocytesAdipose CellAdipose tissueAdoptive TransferAdult-Onset Diabetes MellitusAge MonthsAgingAnti-CD20 AntibodyAntibodiesAquadiolB blood cellsB cellB cell differentiationB cellsB lymphocyte differentiationB-Cell DeficiencyB-CellsB-LymphocytesB-cellBasal Transcription FactorBasal transcription factor genesBioenergeticsBody CompositionBody Weight decreasedBody fatBone MarrowBone Marrow Reticuloendothelial SystemCardiovascular DiseasesCell BodyCell Communication and SignalingCell FunctionCell LineageCell PhysiologyCell ProcessCell SignalingCellsCellular FunctionCellular PhysiologyCellular ProcessCognitive DisturbanceCognitive ImpairmentCognitive declineCognitive function abnormalCytotoxic cellD-GlucoseDataDevelopmentDextroseDiet rich in fats and sugarsDimenformonDiogynDiogynetsDiseaseDisorderDisturbance in cognitionER-BETAERalphaERbetaERαERβESR-BETAESR1ESR1 geneESR2ESR2 geneESRBESTRBEnergy ExpenditureEnergy MetabolismEnvironmentEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessEstraceEstradiolEstradiol Receptor alphaEstradiol Receptor αEstradiol-17 betaEstradiol-17betaEstraldineEstrogen Receptor 1Estrogen Receptor 2Estrogen Receptor alphaEstrogen Receptor betaEstrogen Receptor αEstrogen Receptor βEstrogensEventFat CellsFatty TissueFemaleFlow CytofluorometriesFlow CytofluorometryFlow CytometryFlow MicrofluorimetryFlow MicrofluorometryGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenetic TranscriptionGeroscienceGlucoseGoalsHumanImmuneImmune RegulatorsImmune infiltratesImmunesImmunocompetentImmunomodulationImmunomodulatorsImpaired cognitionImpairmentInfiltrationInflammationInflammatoryInsulin ResistanceIntermediary MetabolismInterventionIntracellular Communication and SignalingK lymphocyteKO miceKetosis-Resistant Diabetes MellitusKnock-outKnock-out MiceKnockoutKnockout MiceLigandsLipocytesMature LipocyteMature fat cellMaturity-Onset Diabetes MellitusMeasuresMediatingMediatorMenopauseMetabolicMetabolic ProcessesMetabolic dysfunctionMetabolismMiceMice MammalsModelingModern ManMolecularMorphologyMurineMusNIDDMNK CellsNR3A1NR3A2Natural Killer CellsNon-Insulin Dependent DiabetesNon-Insulin-Dependent Diabetes MellitusNoninsulin Dependent DiabetesNoninsulin Dependent Diabetes MellitusNull MouseObesityOophorectomyOvarianOvariectomyOvocyclinOvocylinPerimenopausalPerimenopausePhasePhenotypePopulationPost-MenopausePost-menopausal PeriodPostmenopausal PeriodPostmenopauseProductionProgynonRNA ExpressionRepressionRiskRoleSignal TransductionSignal Transduction SystemsSignalingSlow-Onset Diabetes MellitusSpleenSpleen Reticuloendothelial SystemStable Diabetes MellitusSubcellular ProcessT2 DMT2DT2DMTamoxifenTestingTherapeutic EstradiolTherapeutic EstrogenTissue ExpansionTranscriptionTranscription Factor Proto-OncogeneTranscription factor genesType 2 Diabetes MellitusType 2 diabetesType II Diabetes MellitusType II diabetesVisceralWeightWeight GainWeight IncreaseWeight LossWeight ReductionWild Type MouseWomanWomen's prevalenceadiposeadiposityadult onset diabetesafter menopauseage associated diseaseage associated disorderage associated impairmentage dependent diseaseage dependent disorderage dependent impairmentage related human diseaseage-related diseaseage-related disorderage-related impairmentagedantagonismantagonistanti-CD20biological signal transductionbody weight gainbody weight increasebody weight lossbone cellburden of diseaseburden of illnesscardiovascular disordercognitive dysfunctioncognitive losscorpulencecyclohexenecytokinedeprivationdesigndesigningdevelopmentaldiabetes riskdiet high in fat and sugardiet-associated obesitydiet-induced obesitydiet-related obesitydisease burdenepigeneticallyestrogen disruptingestrogen disruptionestrogenic disruptionexperienceexperimentexperimental researchexperimental studyexperimentsfasting glucosefemale gonadectomyfemale prevalenceflexibilityflexibleflow cytophotometryfollowing menopausegeroscientificglucose metabolismhigh-fat/sugar diethumoral immunity deficiencyimmune cell infiltrateimmune competentimmune modulationimmune modulatorsimmune regulationimmunologic reactivity controlimmunomodulatoryimmunomodulatory moleculesimmunoregulationimmunoregulatorimmunoregulatoryimmunoregulatory moleculesimprovedinflammation markerinflammatory markerinsulin resistantinsulin sensitivityinsulin toleranceketosis resistant diabetesmalematurity onset diabetesmenopause transitionmouse modelmurine modelnovelobesity developmentpast menopauseperi-menopausalperi-menopausepost-menopausalpostmenopausalpostmenopausal statusprevalence among femalesprevalence among womenprevalence in femalesprevalence in womenprevalent among femalesprevalent among womenprevalent in femalesprevalent in womenpreventpreventingprogramsscRNA sequencingscRNA-seqsingle cell RNA-seqsingle cell RNAseqsingle cell expression profilingsingle cell transcriptomic profilingsingle-cell RNA sequencingsocial rolesubcutaneoussubdermalsuccesssystemic inflammationsystemic inflammatory responsetraffickingtranscription factortranscriptomicstransition to menopausetransitional menopausetreatment grouptype 2 DMtype II DMtype two diabetesweightswhite adipose tissuewildtype mousewt gainwt-lossyellow adipose tissue♀♂
Description preview
ABSTRACT
Obesity is prevalent in women in the peri- and postmenopausal years. After menopause, women experience
greater risks of many diseases, including cardiovascular disease and type 2 diabetes (T2D). Estrogen (E2) loss
alters body composition by increasing and redistributing body fat, and decreasing energy expenditure and
metabolic…
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