Calcium and vitamin D: what is known about the effects on growing bone.
The objective of these investigations was to determine if the receptor-dependent effects of 1,25-dihydroxyvitamin D were essential for normal skeletal growth. Mice with targeted ablation of the vitamin D receptor were engineered, and the skeletal consequences of vitamin D receptor ablation were studied in the presence of normal and abnormal mineral ion homeostasis. Prevention of abnormal mineral ion homeostasis resulted in the development of a normal skeleton in the absence of a functional vitamin D receptor. The metabolic cause of rickets was found to be hypophosphatemia. The major receptor-dependent actions of 1,25-dihydroxyvitamin D on skeletal development are indirect and are a reflection of the role of this hormone on intestinal calcium absorption.
Demay
Marie B
MB
Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. demay@helix.mgh.harvard.edu
Sabbagh
Yves
Y
Carpenter
Thomas O
TO
D000818:Animals; D001846:Bone Development / Q000502:physiology*; D002136:Calcium, Dietary / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D019902:Chondrocytes / Q000378:metabolism; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D053098:Familial Hypophosphatemic Rickets / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D007785:Lactose / Q000378:metabolism; D051379:Mice; D023421:Models, Animal; D010758:Phosphorus / Q000378:metabolism; D014807:Vitamin D / Q000031:analogs & derivatives* / Q000378:metabolism; D000097568:Matrix Gla Protein
D002136:Calcium, Dietary; D002135:Calcium-Binding Proteins; D016326:Extracellular Matrix Proteins; D007785:Lactose; D010758:Phosphorus; D014807:Vitamin D; D000097568:Matrix Gla Protein; C097949:1,25-dihydroxyvitamin D