grant

Loss of insulin signaling across functional pancreas compartments as a major pathogenic mechanism underlying diabetic exocrine pancreatopathy

Organization UNIVERSITY OF MIAMI SCHOOL OF MEDICINELocation CORAL GABLES, UNITED STATESPosted 12 Jan 2024Deadline 31 Dec 2028
NIHUS FederalResearch GrantFY202621+ years oldASCVDAcinar CellAciner CellsAcuteAddressAdultAdult HumanAdventitial CellAffectAnatomic SitesAnatomic structuresAnatomyAtherosclerosisAtherosclerotic Cardiovascular DiseaseB9 endocrine pancreasBeta CellBlood VesselsBlood flowBody TissuesBrittle Diabetes MellitusCausalityCell BodyCell Communication and SignalingCell FunctionCell PhysiologyCell ProcessCell SignalingCellsCellular FunctionCellular PhysiologyCellular ProcessChronicDataDedicationsDeteriorationDevelopmentDiabetes MellitusDiseaseDisorderDysfunctionEndocrineEndocrine PancreasEndothelial CellsEnteralEntericEtiologyExocrine pancreasFibrosisFunctional disorderGene ExpressionGeneticGoalsHistologicHistologicallyHumanHumulin RIDDMImpairmentIndividualInfiltrationInflammationInflammatoryInsulinInsulin CellInsulin ReceptorInsulin Receptor Protein-Tyrosine KinaseInsulin Secreting CellInsulin Signaling PathwayInsulin-Dependent Diabetes MellitusInsulin-Dependent Tyrosine Protein KinaseIntracellular Communication and SignalingIslands of LangerhansIslets of LangerhansJuvenile-Onset Diabetes MellitusKO miceKetosis-Prone Diabetes MellitusKnock-out MiceKnockout MiceKnowledgeMeasuresMiceMice MammalsMissionModelingModern ManMurineMusNational Institutes of HealthNerve CellsNerve Impulse TransmissionNerve TransmissionNerve UnitNesidioblastsNeural CellNeurocyteNeuronal TransmissionNeuronsNovolin RNull MouseOrgan DonorPancreasPancreaticPancreatic IsletsPars endocrina pancreatisPathogenicityPathologicPatientsPericapillary CellPericytesPerivascular CellPersonsPhysiopathologyPrevalenceRegular InsulinRegulationRegulatory ElementResearchResearch SpecimenRoleRouget CellsSecretory CellSignal TransductionSignal Transduction SystemsSignalingSiteSliceSpecimenSubcellular ProcessSudden-Onset Diabetes MellitusT1 DMT1 diabetesT1DT1DMTestingTissuesType 1 Diabetes MellitusType 1 diabetesType I Diabetes MellitusUnited States National Institutes of Healthadulthoodatheromatosisatherosclerotic diseaseatherosclerotic vascular diseaseautoimmune attackautoimmune destructionautoimmune pathogenesisaxon signalingaxon-glial signalingaxonal signalingbiological signal transductionblood glucose regulationcausationcholinergicchronic pancreatitisdevelop therapydevelopmentaldiabetesdiabeticdisease causationexocrine pancreaticglia signalingglial signalingglucose controlglucose homeostasisglucose regulationin vivoinsightinsulin dependent diabetesinsulin dependent type 1insulin secretioninsulin signalingintervention developmentisletjuvenile diabetesjuvenile diabetes mellitusketosis prone diabetesmouse modelmurine modelnerve signalingneuralneural signalingneuronalneuronal signalingneurotransmissionnutrient absorptionparacrinepathophysiologyrecurrent pancreatitisresponsesocial roletherapy developmenttooltreatment developmenttype I diabetestype one diabetesvascularβ-cellβ-cellsβCell
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PROJECT SUMMARY ABSTRACT
The exocrine pancreas of patients with type 1 diabetes is smaller than the pancreas of healthy subjects and

shows histological anomalies such as fibrosis, fatty degeneration, inflammatory cell infiltration and

atherosclerosis. The histological features associated with diabetes are so specific that they have been defined

as…

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Loss of insulin signaling across functional pancreas compartments as a major pathogenic mechanism underlying diabetic ex | Dev Procure