title: Vitamin D activities and metabolic bone disease.
abstract: 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.
authors.affiliation: 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.
authors.forename: Jackson W
authors.initials: JW
authors.lastname: Ryan
authors.forename: Paul H
authors.initials: PH
authors.lastname: Anderson
authors.forename: Andrew G
authors.initials: AG
authors.lastname: Turner
authors.forename: Howard A
authors.initials: HA
authors.lastname: Morris
mesh_terms: D015090:25-Hydroxyvitamin D3 1-alpha-Hydroxylase / Q000235:genetics / Q000378:metabolism; D015519:Bone Density; D001842:Bone and Bones / Q000378:metabolism* / Q000473:pathology; D002113:Calcification, Physiologic; D002118:Calcium / Q000378:metabolism; D002648:Child; D005786:Gene Expression Regulation; D006801:Humans; D010018:Osteomalacia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D010024:Osteoporosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D010710:Phosphates / Q000378:metabolism; D018167:Receptors, Calcitriol / Q000235:genetics / Q000378:metabolism; D014807:Vitamin D / Q000031:analogs & derivatives* / Q000378:metabolism; D014808:Vitamin D Deficiency / Q000150:complications / Q000378:metabolism* / Q000473:pathology
chemical_list: D010710:Phosphates; D018167:Receptors, Calcitriol; D014807:Vitamin D; C097949:1,25-dihydroxyvitamin D; C104450:25-hydroxyvitamin D; D015090:25-Hydroxyvitamin D3 1-alpha-Hydroxylase; D002118:Calcium
keywords: 25-Hydroxyvitamin D 1α-hydroxylase (CYP27B1); Dietary calcium; Fracture; Osteomalacia; Osteoporosis; Vitamin D