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Clin Chim Acta. 2013 Oct 21;425:148-52. doi: 10.1016/j.cca.2013.07.024. Epub 2013 Jul 30.

Vitamin D activities and metabolic bone disease.

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School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia; Chemical Pathology Directorate and Hanson Institute, SA Pathology, Adelaide South Australia 5000, Australia.


Vitamin D activity requires an adequate vitamin D status as indicated by the serum level of 25-hydroxyvitamin D and appropriate expression of genes coding for vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase, the enzyme which converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. Vitamin D deficiency contributes to the aetiology of osteomalacia and osteoporosis. The key element of osteomalacia, or rickets in children, is a delay in mineralization. It can be resolved by normalisation of plasma calcium and phosphate homeostasis independently of vitamin D activity. The well characterised endocrine pathway of vitamin D metabolism generates plasma 1,25-dihydroxyvitamin D and these endocrine activities are solely responsible for vitamin D regulating plasma calcium and phosphate homeostasis and protection against osteomalacia. In contrast, a large body of clinical data indicate that an adequate serum 25-hydroxyvitamin D level improves bone mineral density protecting against osteoporosis and reducing fracture risk. Recent research demonstrates that the three major bone cell types have the capability to metabolise 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D to activate the vitamin D receptor and modulate gene expression. Dietary calcium intake interacts with vitamin D metabolism at both the renal and bone tissue levels to direct either a catabolic action on bone through the endocrine system when calcium intake is inadequate or an anabolic action through a bone autocrine or paracrine system when calcium intake is sufficient.


25-Hydroxyvitamin D 1α-hydroxylase (CYP27B1); Dietary calcium; Fracture; Osteomalacia; Osteoporosis; Vitamin D

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