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Calcium and vitamin D: what is known about the effects on growing bone

Marie B Demay1, Yves Sabbagh, Thomas O Carpenter

  • 1Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. demay@helix.mgh.harvard.edu

Pediatrics
|March 3, 2007
PubMed

Insights

Vitamin D receptor (VDR) is not essential for skeletal growth. Normal skeletal development occurred even without a functional VDR when mineral ion homeostasis was maintained, indicating indirect effects.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Mineral Metabolism

Background:

  • 1,25-dihydroxyvitamin D is a key hormone regulating calcium and phosphate.
  • The vitamin D receptor (VDR) mediates the effects of this hormone.
  • Its role in skeletal growth, particularly receptor-dependent effects, requires clarification.

Purpose of the Study:

  • To determine if VDR-dependent effects of 1,25-dihydroxyvitamin D are essential for normal skeletal growth.
  • To investigate skeletal development in VDR-ablated mice under varying mineral ion homeostasis conditions.

Main Methods:

  • Engineered mice with targeted ablation of the vitamin D receptor.
  • Studied skeletal consequences in the presence of normal and abnormal mineral ion homeostasis.
  • Analyzed the metabolic basis of rickets, specifically hypophosphatemia.

Main Results:

  • Mice lacking a functional VDR developed normal skeletons when mineral ion homeostasis was preserved.
  • Abnormal mineral ion homeostasis led to skeletal abnormalities.
  • Hypophosphatemia was identified as the metabolic cause of rickets in this model.

Conclusions:

  • Receptor-dependent actions of 1,25-dihydroxyvitamin D on skeletal development are primarily indirect.
  • The hormone's major skeletal influence is mediated through its role in intestinal calcium absorption.
  • Maintaining mineral ion balance is crucial for skeletal integrity, independent of VDR signaling.

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