X-linked Hypophosphatemia (XLH) is a disorder of excessive fibroblast-growth factor 23 (FGF23) production in which the suppressed renal 1,25(OH)2D production, via raised CYP24A1-mediated catabolism, contributes to the development of rickets. While the role of 1,25(OH)2D replacement therapy in XLH has been well studied, it is unknown whether restoring serum 25(OH)D levels itself is beneficial in treating XLH rickets. 3-week-old male HYP mice (n=8/group) were fed one of four diets containing Vitamin D at 1000IU/kg (control) or 20,000IU/kg (HD) phosphate at 0.6% (NP) or 1.25% (HP) for 9 weeks. Both HD and HD+HP fed mice resulted in the 2-fold and 3.5-fold increase in serum 25(OH)D levels respectively when compared to control- or HP-fed mice levels (P<0.0001). All HP-fed mice increased serum phosphate levels by at least 20% when compared to control- and HD-fed mice. Serum Ca and PTH concentrations were unchanged and FGF23 increased across all dietary groups. In HP-fed mice, improved bone indices were observed with a 42% reduction in femoral growth plate width (P<0.05), 1.5-fold increased trabecular BV (P<0.01), and 1.6-fold increase in BMD (P<0.0001). HD-fed mice also demonstrated improved bone indices, with a comparable 40% reduction in growth plate width, and a 1.6-fold increase in both trabecular BV and BMD (P<0.0001). However, only in HD mice did femoral trabecular BV/TV increase by 2 fold (P<0.0001,) driven by a 12% increase in thickness (P<0.001), 77% increase in number (P<0.0001), 23% reduction in trabecular separation (P<0.0001), and a 38% decrease in osteoid volume (P<0.001). Additionally, Cortical BV increased by 25%, and cortical porosity decreased by 6% (P<0.01). Thus, vitamin D supplementation alone fed to HYP mice promotes bone mineral accrual despite hypophosphatemia, suggesting that vitamin D supplementation is a safe therapy for the treatment of XLH.