The present study was designed to investigate whether enhanced bone formation due to intermittent PTH administration is dependent on vitamin D metabolites. Forty-eight female Sprague-Dawley rats were randomized into four groups: 1) vitamin D-sufficient, saline-injected (�D Sal); 2) vitamin D-sufficient, human (h) PTH-(1–38)-treated (�D PTH); 3) vitamin D-deficient, saline-injected (�D Sal); and 4) vitamin D-deficient, hPTH-(1–38)-treated (�D PTH) animals. The �D diet contained 2 % calcium (Ca), 1.25 % phosphorus (P), and 20 % lactose to maintain normocalcemia and normophosphatemia despite vitamin D deficiency. The �D diet contained 0.8 % Ca, 0.5 % P, 20 % lactose, and 1000 IU/kg vitamin D. After 45 days of either diet, the rats were injected with 50 �g/kg BW PTH or saline, sc, daily for 2 weeks. Serum Ca, Mg, P, albumin, and creatinine were similar in al
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