Fibroblast Growth Factor 23 (FGF23) and Disorders of Phosphate Metabolism
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Review Article Fibroblast Growth Factor 23 (FGF23) and Disorders of Phosphate Metabolism Tasuku Saito1 and Seiji Fukumoto2 1 Department
of Pediatrics, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan of Nephrology & Endocrinology, Department of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
2 Division
Correspondence should be addressed to Seiji Fukumoto, [email protected] Received 28 May 2009; Accepted 27 July 2009 Recommended by Ali S Calikoglu 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. Copyright © 2009 T. Saito and S. Fukumoto. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
2. Structure and Function of FGF23
It is well known that serum calcium (Ca) level is regulated within a narrow range by actions of two calciumregulating hormones, parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2 D]. In contrast, while derangements in serum phosphate level result in rickets/osteomalacia or ectopic calcification, the regulatory mechanisms of serum phosphate have been largely unknown. Because PTH and 1,25(OH)2 D can affect serum phosphate level, it has been unclear whether there is a tight mechanism of serum phosphate level regulated by a specific phosphateregulating hormone. However, the identification of fibroblast growth factor 23 (FGF23) and subsequent studies certainly changed this view. FGF23 works as a phosphate-regulating hormone and aberrant functions of FGF23 result in several diseases. Here, we briefly review the physiological and pathophysiological roles of FGF23.
FGF family members are now defined as humoral factorswhich have FGF homology region characterized by β-trefoil structure. FGF23 was identified as the last member of FGF family [1] and belongs to the FGF19 subfamily as well as FGF19 and FGF21 [2]. FGF23 is produced as a peptide with 251 amino acids by bone [3, 4]. There is a signal pepti
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