Fibroblast Growth Factor 23 (FGF23) and Disorders of Phosphate Metabolism
Open Access
- 1 January 2009
- journal article
- review article
- Published by Springer Science and Business Media LLC in International Journal of Pediatric Endocrinology
- Vol. 2009 (1), 1-6
- https://doi.org/10.1155/2009/496514
Abstract
Derangements in serum phosphate level result in rickets/osteomalacia or ectopic calcification indicating that healthy people without these abnormalities maintain serum phosphate within certain ranges. These results indicate that there must be a regulatory mechanism of serum phosphate level. Fibroblast growth factor 23 (FGF23) was identified as the last member of FGF family. FGF23 is produced by bone and reduces serum phosphate level by suppressing phosphate reabsorption in proximal tubules and intestinal phosphate absorption through lowering 1,25-dihydroxyvitamin D level. It has been shown that excess and deficient actions of FGF23 result in hypophosphatemic rickets/osteomalacia and hyperphosphatemic tumoral calcinosis, respectively. These results indicate that FGF23 works as a hormone, and several disorders of phosphate metabolism can be viewed as endocrine diseases. It may become possible to treat patients with abnormal phosphate metabolism by pharmacologically modifying the activity of FGF23.Keywords
This publication has 43 references indexed in Scilit:
- Hypophosphatemia induced by intravenous administration of saccharated ferric oxide: Another form of FGF23-related hypophosphatemiaBone, 2009
- FGF23 Elevation and Hypophosphatemia after Intravenous Iron Polymaltose: A Prospective StudyJournal of Clinical Endocrinology & Metabolism, 2009
- Iron polymaltose-induced FGF23 elevation complicated by hypophosphataemic osteomalaciaAnnals of Clinical Biochemistry: International Journal of Laboratory Medicine, 2009
- Pathogenic role of Fgf23 in Dmp1-null miceAmerican Journal of Physiology-Endocrinology and Metabolism, 2008
- Clinical usefulness of measurement of fibroblast growth factor 23 (FGF23) in hypophosphatemic patients: Proposal of diagnostic criteria using FGF23 measurementBone, 2008
- A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosisJCI Insight, 2007
- Klotho converts canonical FGF receptor into a specific receptor for FGF23Nature, 2006
- Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolismNature Genetics, 2006
- A Deleterious Mutation in SAMD9 Causes Normophosphatemic Familial Tumoral CalcinosisAmerican Journal of Human Genetics, 2006
- FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate HomeostasisJournal of Bone and Mineral Research, 2004