Figure 1. Dietary phosphate supplementation aggravates FGF23 excess and bone microarchitecture in Dmp1^KO mice.

Serum levels of (A) total FGF23 (cFGF23), (B) intact FGF23 (iFGF23), (C) intact to total FGF23 ratio (i/c FGF23), (D) parathyroid hormone (PTH), (E) 1,25-dihydroxyvitamin D [1,25(OH)₂D], (F) calcium (Ca²⁺), and (G) phosphate (Pi); (H) fractional excretion of Pi (FePi); (I) body weight, (J) tail length, and (K) femur length; 3D-μCT scan reconstruction of (L) distal femur trabecular metaphysis (scale bar = 200 μm); (M) midshaft femur cortical diaphysis (scale bar = 500 μm); (N) 2D μCT analysis of cortical bone porosity (scale bar = 100 μm); (O) red fluorescence microscopy imaging of alizarin red S–stained (ARS-stained) mineralization fronts; (P) bright-field microscopy imaging of modified trichrome Goldner staining; and (Q) tartrate-resistant acidic phosphatase (TRAcP) staining of longitudinal histology sections of distal femur (scale bar = 100 μm for ARS, 500 μm for Goldner and TRAcP). All analyses were performed in 12-week-old WT (n ≥ 5) and Dmp1^KO (n ≥ 5) mice fed a diet containing 0.7% Pi (normal Pi, NP) or 2% Pi (high Pi, HP) from 6 to 12 weeks of age. Values are expressed as mean ± SEM; P < 0.05 vs. ^aNP-WT, ^bHP-WT, ^cNP-Dmp1^KO; P < 0.1 vs. ^dNP-WT, ^eHP-WT. Statistical tests were ANOVA test followed by post hoc t tests and multiple-testing correction using Holm-Bonferroni method.