2010
Circulating Levels of Soluble Klotho and FGF23 in X-Linked Hypophosphatemia: Circadian Variance, Effects of Treatment, and Relationship to Parathyroid Status
Carpenter TO, Insogna KL, Zhang JH, Ellis B, Nieman S, Simpson C, Olear E, Gundberg CM. Circulating Levels of Soluble Klotho and FGF23 in X-Linked Hypophosphatemia: Circadian Variance, Effects of Treatment, and Relationship to Parathyroid Status. The Journal Of Clinical Endocrinology & Metabolism 2010, 95: e352-e357. PMID: 20685863, PMCID: PMC2968736, DOI: 10.1210/jc.2010-0589.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAge FactorsAgedBone Density Conservation AgentsCalcitriolChildCircadian RhythmEnzyme-Linked Immunosorbent AssayFamilial Hypophosphatemic RicketsFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGenetic Diseases, X-LinkedGlucuronidaseHumansKlotho ProteinsMaleMiddle AgedParathyroid HormonePhosphatesVitamin DConceptsSerum KlothoSerum FGF23Higher klotho levelsHospital research unitRenal phosphate handlingAcademic medical centerEffect of treatmentFibroblast growth factorKlotho levelsPTH secretionMedical therapySoluble KlothoDihydroxyvitamin DFGF23 regulationPhosphate handlingMedical CenterFGF23KlothoXLHCircadian variationGrowth factorPTHAdultsHypophosphatemiaTherapy
2009
Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse
Brownstein CA, Zhang J, Stillman A, Ellis B, Troiano N, Adams DJ, Gundberg CM, Lifton RP, Carpenter TO. Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse. Endocrinology 2009, 151: 492-501. PMID: 19952276, PMCID: PMC2817612, DOI: 10.1210/en.2009-0564.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCrosses, GeneticDNA PrimersDNA-Binding ProteinsFamilial Hypophosphatemic RicketsFemaleFemurFibroblast Growth Factor-23Genetic Diseases, X-LinkedGenotypeGlucuronidaseHeterozygoteHomozygoteHumansKlotho ProteinsMaleMiceMice, KnockoutNuclear ProteinsPolymerase Chain ReactionTibiaTomography, X-Ray ComputedTranscription FactorsConceptsTrabecular bone densityHyp miceBone densityGreater trabecular bone volume fractionFibroblast growth factor 23Serum PTH levelsDihydroxyvitamin D levelsGrowth factor 23Vitamin D metabolismTrabecular bone volume fractionDouble knockout miceKlotho null miceFGF23 effectsKlotho lossPhosphaturic activityPTH levelsFGF23 actionFGF23 levelsBone volume fractionFactor 23D metabolismD levelsFGF receptor 1Osteoid volumeBone volumeNuclear Isoforms of Fibroblast Growth Factor 2 Are Novel Inducers of Hypophosphatemia via Modulation of FGF23 and KLOTHO*
Xiao L, Naganawa T, Lorenzo J, Carpenter TO, Coffin JD, Hurley MM. Nuclear Isoforms of Fibroblast Growth Factor 2 Are Novel Inducers of Hypophosphatemia via Modulation of FGF23 and KLOTHO*. Journal Of Biological Chemistry 2009, 285: 2834-2846. PMID: 19933269, PMCID: PMC2807337, DOI: 10.1074/jbc.m109.030577.Peer-Reviewed Original ResearchAbsorptiometry, PhotonAnimalsCell NucleusFibroblast Growth Factor 2Fibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHomeostasisHumansHypophosphatemiaIsomerismKidneyKlotho ProteinsMaleMiceMice, TransgenicMolecular WeightOsteoblastsOsteomalaciaPhenotypePhosphatesPromoter Regions, GeneticSkullSodium-Phosphate Cotransporter Proteins, Type IIaX-Ray Microtomography
2008
A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism
Brownstein CA, Adler F, Nelson-Williams C, Iijima J, Li P, Imura A, Nabeshima Y, Reyes-Mugica M, Carpenter TO, Lifton RP. A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 3455-3460. PMID: 18308935, PMCID: PMC2265125, DOI: 10.1073/pnas.0712361105.Peer-Reviewed Original ResearchConceptsHypophosphatemic ricketsAlpha-KlothoExcessive renal lossPhosphate levelsParathyroid massRenal failureRenal osteodystrophyFGF23 levelsMajor complicationsParathyroid hyperplasiaKidney failureRenal lossBeta-glucuronidase activityNormal responseHyperparathyroidismEnergy homeostasisRicketsBone formationSkeletal abnormalitiesPhysiologic processesPhosphate homeostasisHyperphosphatemiaPatientsHyperplasiaBone defects