HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

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.
AuthorsJackson W Ryan, Paul H Anderson, Andrew G Turner, Howard A Morris
JournalClinica chimica acta; international journal of clinical chemistry (Clin Chim Acta) Vol. 425 Pg. 148-52 (Oct 21 2013) ISSN: 1873-3492 [Electronic] Netherlands
PMID23911750 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Copyright© 2013.
Chemical References
  • Phosphates
  • Receptors, Calcitriol
  • Vitamin D
  • 1,25-dihydroxyvitamin D
  • 25-hydroxyvitamin D
  • 25-Hydroxyvitamin D3 1-alpha-Hydroxylase
  • Calcium
Topics
  • 25-Hydroxyvitamin D3 1-alpha-Hydroxylase (genetics, metabolism)
  • Bone Density
  • Bone and Bones (metabolism, pathology)
  • Calcification, Physiologic
  • Calcium (metabolism)
  • Child
  • Gene Expression Regulation
  • Humans
  • Osteomalacia (etiology, metabolism, pathology)
  • Osteoporosis (etiology, metabolism, pathology)
  • Phosphates (metabolism)
  • Receptors, Calcitriol (genetics, metabolism)
  • Vitamin D (analogs & derivatives, metabolism)
  • Vitamin D Deficiency (complications, metabolism, pathology)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: