2011
Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression
Cheng H, Fan X, Moeckel GW, Harris RC. Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression. Journal Of The American Society Of Nephrology 2011, 22: 1240-1251. PMID: 21737546, PMCID: PMC3137572, DOI: 10.1681/asn.2010111149.Peer-Reviewed Original ResearchConceptsCOX-2 transgenic miceDiabetic nephropathyFoot process effacementCOX-2Transgenic miceGlomerular injuryReceptor expressionHigh glucoseRenin-angiotensin systemMesangial matrix expansionCOX-2 inhibitionWild-type miceCOX-2 inhibitorsCyclooxygenase-2 expressionGlomerular basement membraneStreptozotocin modelProgressive albuminuriaSegmental thickeningMesangial expansionDiabetic mellitusCell injuryAnimal modelsInjuryIncreased expressionNephropathySGLT2 Deletion Improves Glucose Homeostasis and Preserves Pancreatic β-Cell Function
Jurczak MJ, Lee HY, Birkenfeld AL, Jornayvaz FR, Frederick DW, Pongratz RL, Zhao X, Moeckel GW, Samuel VT, Whaley JM, Shulman GI, Kibbey RG. SGLT2 Deletion Improves Glucose Homeostasis and Preserves Pancreatic β-Cell Function. Diabetes 2011, 60: 890-898. PMID: 21357472, PMCID: PMC3046850, DOI: 10.2337/db10-1328.Peer-Reviewed Original ResearchConceptsHigh-fat dietPancreatic β-cell functionΒ-cell functionDb/db backgroundKnockout miceGlucose intoleranceGlucose homeostasisPreserves pancreatic β-cell functionDb/db miceImproved glucose intoleranceGlucose-stimulated insulin secretionRenal glucose excretionPrevention of hyperglycemiaRenal glucose reabsorptionType 2 diabetesDb backgroundPlasma insulin concentrationCotransporter type 2Β-cell massObesity-associated hyperglycemiaΒ-cell deathRegular chowGlucose excretionUrine outputSGLT2 inhibition
2006
Glomerular injury is exacerbated in diabetic integrin α1-null mice
Zent R, Yan X, Su Y, Hudson B, Borza D, Moeckel G, Qi Z, Sado Y, Breyer M, Voziyan P, Pozzi A. Glomerular injury is exacerbated in diabetic integrin α1-null mice. Kidney International 2006, 70: 460-470. PMID: 16775606, DOI: 10.1038/sj.ki.5000359.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasement MembraneCell DivisionCell MovementCells, CulturedCollagen Type IVDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalGlomerular Filtration RateGlucoseGlycation End Products, AdvancedIntegrin alpha1Integrin alpha1beta1MaleMesangial CellsMiceMice, Inbred BALB CMice, KnockoutOxidative StressReactive Oxygen SpeciesConceptsGlomerular filtration rateWild-type miceDiabetic wild-type miceDiabetic nephropathyGlomerular injuryCollagen depositionMesangial cellsGlomerular basement membrane thickeningCollagen IVGlomerular collagen IVIntegrin alpha1-null miceNon-diabetic miceIntegrin α1-null miceBasement membrane thickeningDiabetic mutant mouseGlomerular collagen depositionROS productionCollagen IV productionSTZ injectionWeek 24Renal diseaseGlomerular depositionWeek 36Week 12Filtration rate