FGF23 is not required to regulate fetal phosphorus metabolism but exerts effects within 12 hours after birth

Loss of fibroblast growth factor 23 (FGF23) causes hyperphosphatemia, extraskeletal calcifications, and early mortality; excess FGF23 causes hypophosphatemia with rickets or osteomalacia. However, FGF23 may not be important during fetal development. FGF23 deficiency (Fgf23 null) and FGF23 excess (Phex null) did not alter fetal phosphorus or skeletal parameters.In this study we further tested our hypothesis that FGF23 is not essential for fetal phosphorus regulation but becomes important after birth.Although co-receptor Klotho null adults have extremely high FGF23 concentrations, intact FGF23 was normal in Klotho null fetuses, as were fetal phosphorus and skeletal parameters, and placental and renal expression of FGF23 target genes.Pth/Fgf23 double mutants had the same elevation in serum phosphorus as Pth null fetuses, as compared to normal serum phosphorus in Fgf23 nulls.We examined the postnatal time courses of Fgf23 null, Klotho null, and Phex null mice. Fgf23 nulls and Klotho nulls were normal at birth...