Dietary phosphorus restriction reverses the impaired bone mineralization in vitamin D receptor knockout mice.
Endocrinology
; 142(1): 494-7, 2001 Jan.
Article
em En
| MEDLINE
| ID: mdl-11145614
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fósforo
/
Calcificação Fisiológica
/
Fósforo na Dieta
/
Receptores de Calcitriol
Limite:
Animals
Idioma:
En
Revista:
Endocrinology
Ano de publicação:
2001
Tipo de documento:
Article
País de afiliação:
Japão