Physiological regulation and disorders of phosphate metabolism - Pivotal role of fibroblast growth factor 23

被引：76

作者：

Fukumoto, Seiji ^{[1
]}

机构：

[1] Tokyo Univ Hosp, Dept Internal Med, Div Nephrol & Endocrinol, Tokyo 113, Japan

来源：

INTERNAL MEDICINE | 2008年 / 47卷 / 05期

关键词：

hypophosphatemia; hyperphosphatemia; fibroblast growth factor; Klotho; hormone;

D O I：

10.2169/internalmedicine.47.0730

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Fibroblast growth factor (FGF) 23 has been identified as the last member of FGF family. FGF23 reduces serum phosphate level by suppressing proximal tubular phosphate reabsorption and intestinal phosphate absorption. FGF23 is produced by bone and acts on the kidney through a specific receptor system which is composed of Klotho and certain subtypes of FGF receptors. Excess actions of FGF23 cause several hypophosphatemic diseases characterized by impaired renal phosphate reabsorption and rickets/osteomalacia. In contrast, deficient actions of FGF23 result in hyperphosphatemic tumoral calcinosis with enhanced renal phosphate reabsorption. These results indicate that FGF23 works as a hormone to regulate the serum phosphate level.

引用

页码：337 / 343

页数：7

共 51 条

[11] FGF23 is a hormone-regulating phosphate metabolism - Unique biological characteristics of FGF23 [J].

Fukumoto, Seiji ;

Yamashita, Takeyoshi .

BONE, 2007, 40 (05) :1190-1195

[12] FGF-23 is elevated by chronic hyperphosphatemia [J].

Gupta, A ;

Winer, K ;

Econs, MJ ;

Marx, SJ ;

Collins, MT .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (09) :4489-4492

[13] A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis [J].

Ichikawa, Shoji ;

Lmel, Erik A. ;

Kreiter, Mary L. ;

Yu, Xijie ;

Mackenzie, Donald S. ;

Sorenson, Andrea H. ;

Goetz, Regina ;

Moharnmadi, Moosa ;

White, Kenneth E. ;

Econs, Michael J. .

JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (09) :2684-2691

[14] FGF-23 in patients with end-stage renal disease on hemodialysis [J].

Imanishi, Y ;

Inaba, M ;

Nakatsuka, K ;

Nagasue, K ;

Okuno, S ;

Yoshihara, A ;

Miura, M ;

Miyauchi, A ;

Kobayashi, K ;

Miki, T ;

Shoji, T ;

Ishimura, E ;

Nishizawa, Y .

KIDNEY INTERNATIONAL, 2004, 65 (05) :1943-1946

[15]

Imel EA, 2007, J BONE MINER RES, V22, P520, DOI [10.1359/jbmr.070107, 10.1359/JBMR.070107]

[16] Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis [J].

Inagaki, T ;

Choi, M ;

Moschetta, A ;

Peng, L ;

Cummins, CL ;

McDonald, JG ;

Luo, G ;

Jones, SA ;

Goodwin, B ;

Richardson, JA ;

Gerard, RD ;

Repa, JJ ;

Mangelsdorf, DJ ;

Kliewer, SA .

CELL METABOLISM, 2005, 2 (04) :217-225

[17] Endocrine regulation of the fasting response by PPARα-mediated induction of fibroblast growth factor 21 [J].

Inagaki, Takeshi ;

Dutchak, Paul ;

Zhao, Guixiang ;

Ding, Xunshan ;

Gautron, Laurent ;

Parameswara, Vinay ;

Li, Yong ;

Goetz, Regina ;

Mohammadi, Moosa ;

Esser, Victoria ;

Elmquist, Joel K. ;

Gerard, Robert D. ;

Burgess, Shawn C. ;

Hammer, Robert E. ;

Mangelsdorf, David J. ;

Kliewer, Steven A. .

CELL METABOLISM, 2007, 5 (06) :415-425

[18] Comparison of two assays for fibroblast growth factor (FGF)-23 [J].

Ito, N ;

Fukumoto, S ;

Takeuchi, Y ;

Yasuda, T ;

Hasegawa, Y ;

Takemoto, F ;

Tajima, T ;

Dobashi, K ;

Yamazaki, Y ;

Yamashita, T ;

Fujita, T .

JOURNAL OF BONE AND MINERAL METABOLISM, 2005, 23 (06) :435-440

[19] Impaired negative feedback suppression of bile acid synthesis in mice lacking βKlotho [J].

Ito, S ;

Fujimori, T ;

Furuya, A ;

Satoh, J ;

Nabeshima, Y ;

Nabeshima, Y .

JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (08) :2202-2208

[20] Evolution of the Fgf and Fgfr gene families [J].

Itoh, N ;

Ornitz, DM .

TRENDS IN GENETICS, 2004, 20 (11) :563-569

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