Fibroblast Growth Factor 23 (FGF23) and Disorders of PhosphateMetabolism

被引:39
作者
Saito, Tasuku [1 ]
Fukumoto, Seiji [2 ]
机构
[1] Tokyo Univ Hosp, Dept Pediat, Bunkyo Ku, Tokyo 1138655, Japan
[2] Tokyo Univ Hosp, Dept Med, Div Nephrol & Endocrinol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan
关键词
D O I
10.1155/2009/496514
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Derangements in serum phosphate level result in rickets/ osteomalacia or ectopic calcification indicating that healthy people without these abnormalitiesmaintain serum phosphate within certain ranges. These results indicate that theremust 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 (C) 2009 T. Saito and S. Fukumoto.
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页数:6
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