title: Dietary phosphorus restriction reverses the impaired bone mineralization in vitamin D receptor knockout mice.
abstract: Deficiency of vitamin D, which is required for calcium homeostasis, causes rickets with hypocalcemia and hypophosphatemia, resulting in growth retardation and impaired bone formation. Mice lacking the vitamin D receptor (VDR) develop the typical features of rickets, establishing that VDR plays a role in controlling the actions of vitamin D. Normalization of impaired mineral homeostasis in VDR KO mice fed a diet supplemented with high concentrations of calcium (2%) and phosphorus (1.25%) is reported to reverse the malformation of bone and the growth retardation as well. However, the relationship between mobilization of phosphorus and calcium and nuclear control of vitamin D actions remains unclear. The present study was undertaken to determine the effect of dietary phosphorus on mineral mobilization and bone mineralization. We report here that feeding a diet supplemented with a restricted amount of phosphorus (0.25%) and a normal amount of calcium (0.5%) for 4 weeks reverses the growth retardation and the impaired mineralization in VDR KO mice, as does a high-calcium and high-phosphorus diet (Ca: 2%; P: 1.25%). Thus, the present study suggests that mobilization of calcium and mobilization of phosphorus are differentially regulated through vitamin D-dependent and -independent systems, and that intake of calcium and phosphorus in the proper ratio is important for mineral homeostasis and bone mineralization.
authors.affiliation: Department of Nutritional Science, Tokyo University of Agriculture, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Masuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Nakaya
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: H
authors.initials: H
authors.lastname: Tsurukami
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: S
authors.initials: S
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Yoshizawa
authors.forename: S
authors.initials: S
authors.lastname: Kato
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D002113:Calcification, Physiologic / Q000235:genetics / Q000502:physiology*; D003433:Crosses, Genetic; D005260:Female; D005269:Femur; D006706:Homeostasis; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D010758:Phosphorus / Q000172:deficiency*; D016226:Phosphorus, Dietary; D018167:Receptors, Calcitriol / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D012279:Rickets / Q000235:genetics
chemical_list: D016226:Phosphorus, Dietary; D018167:Receptors, Calcitriol; D010758:Phosphorus