2024
Shifting the paradigm of type 1 diabetes: a narrative review of disease-modifying therapies
O’Donovan A, Gorelik S, Nally L. Shifting the paradigm of type 1 diabetes: a narrative review of disease-modifying therapies. Frontiers In Endocrinology 2024, 15: 1477101. PMID: 39568817, PMCID: PMC11576206, DOI: 10.3389/fendo.2024.1477101.Peer-Reviewed Original ResearchDisease modifying therapiesStages of T1DFood and Drug AdministrationType 1 diabetesLong-term insulin dependenceDestruction of pancreatic beta cellsModifying therapiesDiagnosis of type 1 diabetesClinical diagnosis of T1DClinical diseasePathogenesis of T1DDetection of autoantibodiesDiagnosis of T1DNarrative reviewSymptoms of hyperglycemiaPancreatic beta cellsMechanism of actionAutoimmune conditionsInsulin-DependentPublished trialsGlycemic changesDrug AdministrationInsulin deficiencyTherapyClinical diagnosisStructure, interaction and nervous connectivity of beta cell primary cilia
Müller A, Klena N, Pang S, Garcia L, Topcheva O, Aurrecoechea Duran S, Sulaymankhil D, Seliskar M, Mziaut H, Schöniger E, Friedland D, Kipke N, Kretschmar S, Münster C, Weitz J, Distler M, Kurth T, Schmidt D, Hess H, Xu C, Pigino G, Solimena M. Structure, interaction and nervous connectivity of beta cell primary cilia. Nature Communications 2024, 15: 9168. PMID: 39448638, PMCID: PMC11502866, DOI: 10.1038/s41467-024-53348-5.Peer-Reviewed Original ResearchConceptsPrimary ciliaCell's primary ciliumNon-islet cellsPancreatic beta cellsCiliary pocketSensory organellesAxonemal organizationMotility componentsExtrinsic signalsStructural basisBeta cellsCiliaCell typesExpansion microscopyParacrine signalingIslet innervationCellsIsletsBetaAxonemeOrganellesSignalThree-dimensional reconstructionInteractionEvidence for C-Peptide as a Validated Surrogate to Predict Clinical Benefits in Trials of Disease-Modifying Therapies for Type 1 Diabetes.
Latres E, Greenbaum C, Oyaski M, Dayan C, Colhoun H, Lachin J, Skyler J, Rickels M, Ahmed S, Dutta S, Herold K, Marinac M. Evidence for C-Peptide as a Validated Surrogate to Predict Clinical Benefits in Trials of Disease-Modifying Therapies for Type 1 Diabetes. Diabetes 2024, 73: 823-833. PMID: 38349844, DOI: 10.2337/dbi23-0012.Peer-Reviewed Original ResearchBeta cell functionType 1 diabetesMeasures of beta cell functionDisease-modifying therapiesC-peptideTrials of disease-modifying therapiesClinical benefitCell functionDestruction of pancreatic beta cellsStimulated C-peptideC-peptide levelsEnd-organ complicationsProspective cohort studyAssociated with protectionEnd-organ complications of diabetesChronic autoimmune diseaseClinically Meaningful OutcomesClinical outcome measuresComplications of diabetesClinical trials of disease-modifying therapiesBeta cell preservationDemonstration of efficacyPancreatic beta cellsPeripheral bloodAutoimmune diseasesMechanism of Insulin Action
White M. Mechanism of Insulin Action. 2024, 111-127. DOI: 10.1002/9781119697473.ch9.Peer-Reviewed Original ResearchReceptor tyrosine kinasesTyrosine kinaseGrowth factor signalingSecrete sufficient insulinDysregulated insulin signalingPancreatic beta cellsMuscle insulin resistanceEnvironmental signalsSignal transductionInsulin signalingMuscle-specific deletionSystemic insulin actionSystemic insulin resistanceAdequate insulin responseFactor signalingInsulin-like growth factor signalingPlasma membraneInsulin resistanceInsulin receptorLigand bindingBeta cellsMetabolic stressChronic insulin resistanceGlucose transportTransphosphorylation
2023
Elevated glucose metabolism driving pro-inflammatory response in B cells contributes to the progression of type 1 diabetes
Li Z, Zhao M, Li J, Luo W, Huang J, Huang G, Xie Z, Xiao Y, Huang J, Li X, Zhao B, Zhou Z. Elevated glucose metabolism driving pro-inflammatory response in B cells contributes to the progression of type 1 diabetes. Clinical Immunology 2023, 255: 109729. PMID: 37562723, DOI: 10.1016/j.clim.2023.109729.Peer-Reviewed Original ResearchConceptsType 1 diabetesPro-inflammatory responseB cellsGlucose metabolismCytokine productionAberrant B cell responsesNon-obese diabetic (NOD) micePro-inflammatory cytokine productionHigh blood glucose levelsOnset of diabetesInflammatory cytokine productionAdaptive immune responsesB cell responsesCross-sectional cohortImmune system failureDiabetic mouse modelB cell functionBlood glucose levelsB cell populationsB cell metabolismPancreatic beta cellsB cell proliferationElevated glucose metabolismInsulitis developmentNOD mice
2022
Biomarkers of autoimmunity and beta cell metabolism in type 1 diabetes
Yang M, Kibbey R, Mamula M. Biomarkers of autoimmunity and beta cell metabolism in type 1 diabetes. Frontiers In Immunology 2022, 13: 1028130. PMID: 36389721, PMCID: PMC9647083, DOI: 10.3389/fimmu.2022.1028130.Peer-Reviewed Original ResearchConceptsPosttranslational protein modificationMetabolic pathwaysType 1 diabetesCellular metabolic pathwaysImportant biological functionsAutoimmune diseasesBeta cellsCellular metabolic dysfunctionPancreatic isletsProtein modificationBiological functionsProtein structureInsulin-producing beta cellsBiomarkers of autoimmunityChronic autoimmune diseaseCell metabolismBeta-cell metabolismNumerous autoimmune diseasesPancreatic beta cellsPotential pathological consequencesNormal metabolic pathwaysDisease activityPathological consequencesSpecific autoantigensSpecific autoimmunityCitrullination of glucokinase is linked to autoimmune diabetes
Yang ML, Horstman S, Gee R, Guyer P, Lam TT, Kanyo J, Perdigoto AL, Speake C, Greenbaum CJ, Callebaut A, Overbergh L, Kibbey RG, Herold KC, James EA, Mamula MJ. Citrullination of glucokinase is linked to autoimmune diabetes. Nature Communications 2022, 13: 1870. PMID: 35388005, PMCID: PMC8986778, DOI: 10.1038/s41467-022-29512-0.Peer-Reviewed Original ResearchConceptsGlucose-stimulated insulin secretionResult of inflammationType 1 diabetesBeta-cell metabolismPancreatic beta cellsAutoimmune diabetesNOD miceAutoreactive CD4Inflammatory cytokinesAutoimmune biomarkersInsulin secretionT cellsBeta cellsType 1InflammationBiologic activityReactive oxygen speciesDiabetesPost-translational modificationsDiabetes biomarkersGlycogen synthesisBiomarkersCitrullinationGlucokinaseOxygen speciesTransient Receptor Potential channels (TRP) in GtoPdb v.2022.1
Blair N, Carvacho I, Chaudhuri D, Clapham D, DeCaen P, Delling M, Doerner J, Fan L, Grimm C, Ha K, Jordt S, Julius D, Kahle K, Liu B, McKemy D, Nilius B, Oancea E, Owsianik G, Riccio A, Sah R, Stotz S, Tian J, Tong D, Van den Eynde C, Vriens J, Wu L, Xu H, Yue L, Zhang X, Zhu M. Transient Receptor Potential channels (TRP) in GtoPdb v.2022.1. IUPHAR/BPS Guide To Pharmacology CITE 2022, 2022 DOI: 10.2218/gtopdb/f78/2022.1.Peer-Reviewed Original ResearchTransient receptor potential channelsCongenital stationary night blindnessTRPC channelsStore-operated channelsMost TRP channelsTRP channelsCation channelsMetabotropic glutamate receptor 6Activation of GoHuman TRPM1 mutationsReabsorption of calciumTRPC4/C5Ion channelsDendritic cell migrationLow extracellular sodiumIntracellular calcium storesActivity of TRPV1Layer 5 neuronsMouse prefrontal cortexMucolipidosis type IVGlutamate receptor 6Store-operated mechanismsMain olfactory epitheliumBroad-spectrum agentsPancreatic beta cells
2021
Transient Receptor Potential channels (TRP) in GtoPdb v.2021.3
Blair N, Carvacho I, Chaudhuri D, Clapham D, DeCaen P, Delling M, Doerner J, Fan L, Ha K, Jordt S, Julius D, Kahle K, Liu B, McKemy D, Nilius B, Oancea E, Owsianik G, Riccio A, Sah R, Stotz S, Tian J, Tong D, Van den Eynde C, Vriens J, Wu L, Xu H, Yue L, Zhang X, Zhu M. Transient Receptor Potential channels (TRP) in GtoPdb v.2021.3. IUPHAR/BPS Guide To Pharmacology CITE 2021, 2021 DOI: 10.2218/gtopdb/f78/2021.3.Peer-Reviewed Original ResearchTransient receptor potential channelsCongenital stationary night blindnessTRPC channelsStore-operated channelsMost TRP channelsTRP channelsCation channelsMetabotropic glutamate receptor 6Activation of GoHuman TRPM1 mutationsReabsorption of calciumTRPC4/C5Ion channelsDendritic cell migrationLow extracellular sodiumIntracellular calcium storesActivity of TRPV1Layer 5 neuronsMouse prefrontal cortexMucolipidosis type IVGlutamate receptor 6Main olfactory epitheliumStore-operated mechanismsBroad-spectrum agentsPancreatic beta cells
2020
Dynamic Regulation of JAK-STAT Signaling Through the Prolactin Receptor Predicted by Computational Modeling
Mortlock RD, Georgia SK, Finley SD. Dynamic Regulation of JAK-STAT Signaling Through the Prolactin Receptor Predicted by Computational Modeling. Cellular And Molecular Bioengineering 2020, 14: 15-30. PMID: 33633812, PMCID: PMC7878662, DOI: 10.1007/s12195-020-00647-8.Peer-Reviewed Original ResearchBeta-cell massBeta cellsInsulin-producing beta cellsReceptor internalizationContext of pregnancyPrimary beta cellsJAK-STATPancreatic beta cellsBeta cell expansionBeta-cell survivalSTAT5 activationProlactin receptor signalingINS-1 cellsGestational diabetesInsulin resistanceReceptor upregulationGlucose homeostasisBiphasic responseA Human Pluripotent Stem Cell-based Platform to Study SARS-CoV-2 Tropism and Model Virus Infection in Human Cells and Organoids
Yang L, Han Y, Nilsson-Payant BE, Gupta V, Wang P, Duan X, Tang X, Zhu J, Zhao Z, Jaffré F, Zhang T, Kim TW, Harschnitz O, Redmond D, Houghton S, Liu C, Naji A, Ciceri G, Guttikonda S, Bram Y, Nguyen DT, Cioffi M, Chandar V, Hoagland DA, Huang Y, Xiang J, Wang H, Lyden D, Borczuk A, Chen HJ, Studer L, Pan FC, Ho DD, tenOever BR, Evans T, Schwartz RE, Chen S. A Human Pluripotent Stem Cell-based Platform to Study SARS-CoV-2 Tropism and Model Virus Infection in Human Cells and Organoids. Cell Stem Cell 2020, 27: 125-136.e7. PMID: 32579880, PMCID: PMC7303620, DOI: 10.1016/j.stem.2020.06.015.Peer-Reviewed Original ResearchConceptsSARS-CoV-2 infectionHuman disease-relevant cellsSARS-CoV-2 tropismCOVID-19 pathophysiologyExpression of chemokinesRecent clinical studiesHuman pancreatic beta cellsCOVID-19SARS-CoV-2Pancreatic beta cellsLiver organoidsPancreatic endocrine cellsRespiratory failureDopaminergic neuronsClinical studiesPrimary human isletsVirus infectionAutopsy samplesBeta cellsHuman isletsEndocrine cellsOrgan systemsInfectionCholangiocyte organoidsDisease-relevant cellsDynamin Function in Exocytosis and Endocytosis Coupling of Dense-Core Vesicles in Pancreatic Beta Cells
Fan F, Wendlick J, Tamarina N, Wu Y, Ferguson S, Philipson L, De Camilli P, Lou X. Dynamin Function in Exocytosis and Endocytosis Coupling of Dense-Core Vesicles in Pancreatic Beta Cells. Biophysical Journal 2020, 118: 488a. DOI: 10.1016/j.bpj.2019.11.2700.Peer-Reviewed Original Research
2019
Transient Receptor Potential channels (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database
Blair N, Carvacho I, Chaudhuri D, Clapham D, DeCaen P, Delling M, Doerner J, Fan L, Ha K, Jordt S, Julius D, Kahle K, Liu B, McKemy D, Nilius B, Oancea E, Owsianik G, Riccio A, Sah R, Stotz S, Tian J, Tong D, Van den Eynde C, Vriens J, Wu L, Xu H, Yue L, Zhang X, Zhu M. Transient Receptor Potential channels (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database. IUPHAR/BPS Guide To Pharmacology CITE 2019, 2019 DOI: 10.2218/gtopdb/f78/2019.4.Peer-Reviewed Original ResearchCongenital stationary night blindnessTRPC channelsStore-operated channelsMost TRP channelsTRP channelsCation channelsMetabotropic glutamate receptor 6Activation of GoHuman TRPM1 mutationsReabsorption of calciumTRPC4/C5Ion channelsDendritic cell migrationIntracellular calcium storesLow extracellular sodiumLayer 5 neuronsTransient receptor potential channelsActivity of TRPV1Mouse prefrontal cortexMucolipidosis type IVGlutamate receptor 6Main olfactory epitheliumStore-operated mechanismsBroad-spectrum agentsPancreatic beta cells
2016
The role of the innate immune system in destruction of pancreatic beta cells in NOD mice and humans with type I diabetes
Tai N, Wong FS, Wen L. The role of the innate immune system in destruction of pancreatic beta cells in NOD mice and humans with type I diabetes. Journal Of Autoimmunity 2016, 71: 26-34. PMID: 27021275, PMCID: PMC4903935, DOI: 10.1016/j.jaut.2016.03.006.Peer-Reviewed Original ResearchConceptsPattern recognition receptorsToll-like receptorsInnate immunityCell autoimmunityAdaptive immunityHuman studiesOrgan-specific autoimmune diseasesT cell-mediated destructionΒ-cellsInsulin-producing pancreatic β-cellsDifferent pattern recognition receptorsCell-mediated destructionDevelopment of T1D.Pathogenesis of T1D.Type 1 diabetesFunctional β-cell massNovel therapeutic strategiesInnate immune responseInnate immune systemΒ-cell massPancreatic beta cellsShape adaptive immunityPancreatic β-cellsIslet β-cellsNOD mice
2013
Arsenic Exposure and Calpain-10 Polymorphisms Impair the Function of Pancreatic Beta-Cells in Humans: A Pilot Study of Risk Factors for T2DM
Díaz-Villaseñor A, Cruz L, Cebrián A, Hernández-Ramírez RU, Hiriart M, García-Vargas G, Bassol S, Sordo M, Gandolfi AJ, Klimecki WT, López-Carillo L, Cebrián ME, Ostrosky-Wegman P. Arsenic Exposure and Calpain-10 Polymorphisms Impair the Function of Pancreatic Beta-Cells in Humans: A Pilot Study of Risk Factors for T2DM. PLOS ONE 2013, 8: e51642. PMID: 23349674, PMCID: PMC3551951, DOI: 10.1371/journal.pone.0051642.Peer-Reviewed Original ResearchConceptsBeta-cell functionLower beta-cell functionSNP-43Risk factorsInsulin sensitivitySNP-44IAs exposureSingle nucleotide polymorphismsChronic exposureCAPN-10Type 2 diabetes mellitusOutcomes of T2DMCalpain-10 polymorphismsGenetic risk factorsPancreatic beta cellsAction of insulinCalpain-10 geneDiabetes mellitusInverse associationInsulin secretionT2DMBeta cellsRisk genotypesArsenic exposurePilot study
2012
Endometrial Stem Cells.
Taylor H. Endometrial Stem Cells. Biology Of Reproduction 2012, 87: 32-32. DOI: 10.1093/biolreprod/87.s1.32.Peer-Reviewed Original ResearchProgenitor stem cellsMesenchymal stem cellsUterine injuryMenstrual cycleMultipotent stem cellsStem cellsAdult progenitor stem cellsPathogenesis of endometriosisEndometrial stem cellsMurine diabetes modelPancreatic beta cellsAsherman's syndromeEndometrial regenerationDopaminergic neuronsDiabetes modelRetrograde fashionMurine modelPeritoneal cavitySex steroidsParkinson's diseaseBeta cellsBone marrowEndometriosisRemarkable regenerative capacityEctopic locations
2008
Reprogramming of Pancreatic β Cells into Induced Pluripotent Stem Cells
Stadtfeld M, Brennand K, Hochedlinger K. Reprogramming of Pancreatic β Cells into Induced Pluripotent Stem Cells. Current Biology 2008, 18: 890-894. PMID: 18501604, PMCID: PMC2819222, DOI: 10.1016/j.cub.2008.05.010.Peer-Reviewed Original ResearchConceptsEmbryonic stem cellsPluripotent stem cellsCell typesIPS cellsStem cellsC-MycTranscription factors Oct4Rare cell typesInduced pluripotent stem cellsCertain cell typesAdult stem cellsInducible lentivirusVitro reprogrammingFactors OCT4Pluripotent cellsEctopic expressionGenetic proofPancreatic β-cellsGerm layersDifferentiated cellsChimeric animalsPluripotency markersDifferentiation stageBeta cellsPancreatic beta cells
2007
Four-turn α-Helical Segment Prevents Surface Expression of the Auxiliary hβ2 Subunit of BK-type Channel*
Lv C, Chen M, Gan G, Wang L, Xu T, Ding J. Four-turn α-Helical Segment Prevents Surface Expression of the Auxiliary hβ2 Subunit of BK-type Channel*. Journal Of Biological Chemistry 2007, 283: 2709-2715. PMID: 17991741, DOI: 10.1074/jbc.m704440200.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCell LineEndoplasmic ReticulumGene ExpressionHumansLarge-Conductance Calcium-Activated Potassium ChannelsMicroscopy, FluorescenceModels, MolecularMolecular Sequence DataMutagenesis, Site-DirectedPatch-Clamp TechniquesProtein Structure, SecondaryProtein SubunitsRatsRecombinant Fusion ProteinsSequence Homology, Amino AcidConceptsBK-type channelsSurface expressionRat chromaffin cellsExtracellular loopPancreatic beta cellsTrafficking mechanismsN-terminusDRG neuronsHelical segmentsToxin sensitivityBeta cellsClamp techniqueHelp of immunofluorescenceAuxiliary beta subunitsAlpha-helical segmentsChromaffin cellsBeta2 subunitBK channelsHbeta2Retention signalChannel regulatorRegulatory mechanismsBeta subunitEndoplasmic reticulumLarge conductanceRegulation of insulin secretion and GLUT4 trafficking by the calcium sensor synaptotagmin VII
Li Y, Wang P, Xu J, Gorelick F, Yamazaki H, Andrews N, Desir GV. Regulation of insulin secretion and GLUT4 trafficking by the calcium sensor synaptotagmin VII. Biochemical And Biophysical Research Communications 2007, 362: 658-664. PMID: 17720139, PMCID: PMC2194288, DOI: 10.1016/j.bbrc.2007.08.023.Peer-Reviewed Original ResearchConceptsGLUT4 trafficSyt VIIPlasma membraneGLUT4 translocationConstitutive expressionSecretory granule exocytosisSkeletal muscle cellsGLUT4 traffickingRegulated exocytosisVoltage-gated potassium channel Kv1.3Vesicular trafficSynaptotagmin VIIGLUT4 presentPotassium channel Kv1.3Calcium sensorIntracellular compartmentsDeletion resultsGlucose-stimulated insulin secretionChannel Kv1.3Granule exocytosisPancreatic beta cellsChannel activityInsulin secretionPancreatic islet cellsMuscle cells
2006
The reciprocal stability of FOXO1 and IRS2 creates a regulatory circuit that controls insulin signaling.
Guo S, Dunn S, White M. The reciprocal stability of FOXO1 and IRS2 creates a regulatory circuit that controls insulin signaling. Endocrinology 2006, 20: 3389-99. PMID: 16916938, DOI: 10.1210/me.2006-0092.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedFibroblastsForkhead Box Protein O1Forkhead Transcription FactorsInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsMiceMice, Mutant StrainsPhosphatidylinositol 3-KinasesPhosphoproteinsProtein KinasesProto-Oncogene Proteins c-aktRecombinant ProteinsSignal TransductionTOR Serine-Threonine KinasesTyrosineConceptsInsulin stimulationWild-type mouse embryo fibroblastsInsulin-receptor substrate IRS1Metastatic mammary tumor cellsProlonged insulin stimulationMouse embryo fibroblastsTranscription factor FOXO1Substrates IRS1FoxO phosphorylationRegulatory circuitsNuclear exclusionWT MEFsTyrosine phosphorylationGene expressionMetabolic regulationEmbryo fibroblastsIRS1 expressionMammary tumor cellsIRS2 expressionCell growthIRS2AktIRS1MEFsPancreatic beta cells
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