Abstract
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.
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