This Article Full Text Full Text (PDF) All Versions of this Article: 90/3/1519    most recent Author Manuscript (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ferrari, S. L. Articles by Rizzoli, R. Search for Related Content PubMed PubMed Citation Articles by Ferrari, S. L. Articles by Rizzoli, R.

Fibroblast Growth Factor-23 Relationship to Dietary Phosphate and Renal Phosphate Handling in Healthy Young Men

Service of Bone Diseases [World Health Organization Collaborating Center for Osteoporosis Prevention], Department of Rehabilitation and Geriatrics, Geneva University Hospital, Geneva 1211, Switzerland

Address all correspondence and requests for reprints to: Serge Ferrari, Service of Bone Diseases, Geneva University Hospital, 24 rue Micheli-du-Crest, Geneva 1211, Switzerland. E-mail: serge.ferrari{at}medecine.unige.ch.

The renal handling of inorganic phosphate (Pi) is controlled not only by PTH, but also by hitherto undetermined mechanisms dependent on phosphate intake. Recently, fibroblast growth factor (FGF)-23 was identified as a novel phosphaturic factor in tumor-induced osteomalacia and autosomal-dominant hypophosphatemic rickets. We hypothesized that phosphate intake could influence FGF-23 concomitantly to the changes in renal Pi handling. Twenty-nine healthy males were subjected to a 5-d low-phosphate diet and a phosphate binder, followed by a high-phosphate diet including supplements. Concomitant modifications in calcium intake allowed minimizing PTH changes in response to dietary phosphate. Serum FGF-23 levels significantly decreased on the low-phosphate diet, then increased with the oral phosphate load. Changes in FGF-23 were positively correlated with changes in 24-h urinary Pi excretion and negatively correlated with changes in the maximal tubular reabsorption of Pi and 1,25(OH)₂D₃ (calcitriol), whereas PTH was not. In multivariate analysis, changes in FGF-23 remained the most significantly correlated to changes in 1,25(OH)₂D₃ and maximal tubular reabsorption of Pi. Moreover, FGF-23 was positively correlated to serum osteocalcin, a marker of osteoblastic activity.

In summary, FGF-23 was inversely related to renal Pi transport and serum calcitriol levels in healthy young men. These data suggest that FGF-23 may be implicated in the physiological regulation of Pi homeostasis in response to dietary phosphate changes, independent of PTH.

This article has been cited by other articles:

				S. Goto, H. Komaba, and M. Fukagawa Pathophysiology of parathyroid hyperplasia in chronic kidney disease: preclinical and clinical basis for parathyroid intervention NDT Plus, August 1, 2008; 1(suppl_3): iii2 - iii8. [Abstract] [Full Text] [PDF]

				J. Danziger The bone-renal axis in early chronic kidney disease: an emerging paradigm Nephrol. Dial. Transplant., May 9, 2008; (2008) gfn260v1. [Full Text] [PDF]

				G. van Boekel, J. Ruinemans-Koerts, F. Joosten, P. Dijkhuizen, A. van Sorge, and H. de Boer Tumor producing fibroblast growth factor 23 localized by two-staged venous sampling Eur. J. Endocrinol., March 1, 2008; 158(3): 431 - 437. [Abstract] [Full Text] [PDF]

				T. Isakova, O. Gutierrez, A. Shah, L. Castaldo, J. Holmes, H. Lee, and M. Wolf Postprandial Mineral Metabolism and Secondary Hyperparathyroidism in Early CKD J. Am. Soc. Nephrol., March 1, 2008; 19(3): 615 - 623. [Abstract] [Full Text] [PDF]

				U. Kunzendorf, B. K. Kramer, W. Arns, J. Braun, J. Grossmann, F. Pietruck, H. Schmidt-Gayk, A. Schwarz, E. Ziegler, H. Sperschneider, et al. Bone disease after renal transplantation Nephrol. Dial. Transplant., February 1, 2008; 23(2): 450 - 458. [Full Text] [PDF]

				L. Thomas and R. Kumar Control of Renal Solute Excretion by Enteric Signals and Mediators J. Am. Soc. Nephrol., February 1, 2008; 19(2): 207 - 212. [Abstract] [Full Text] [PDF]

				P.-A. Westerberg, T. Linde, B. Wikstrom, O. Ljunggren, M. Stridsberg, and T. E. Larsson Regulation of fibroblast growth factor-23 in chronic kidney disease Nephrol. Dial. Transplant., November 1, 2007; 22(11): 3202 - 3207. [Abstract] [Full Text] [PDF]

				D. SITARA Correlation among Hyperphosphatemia, Type II Sodium Phosphate Transporter Activity, and Vitamin D Metabolism in Fgf-23 Null Mice Ann. N.Y. Acad. Sci., November 1, 2007; 1116(1): 485 - 493. [Abstract] [Full Text] [PDF]

				T. Kawata, Y. Imanishi, K. Kobayashi, T. Miki, A. Arnold, M. Inaba, and Y. Nishizawa Parathyroid Hormone Regulates Fibroblast Growth Factor-23 in a Mouse Model of Primary Hyperparathyroidism J. Am. Soc. Nephrol., October 1, 2007; 18(10): 2683 - 2688. [Abstract] [Full Text] [PDF]

				D. Fliser, B. Kollerits, U. Neyer, D. P. Ankerst, K. Lhotta, A. Lingenhel, E. Ritz, F. Kronenberg, and for the MMKD Study Group Fibroblast Growth Factor 23 (FGF23) Predicts Progression of Chronic Kidney Disease: The Mild to Moderate Kidney Disease (MMKD) Study J. Am. Soc. Nephrol., September 1, 2007; 18(9): 2600 - 2608. [Abstract] [Full Text] [PDF]

				S. Canadillas, A. Rodriguez-Benot, and M. Rodriguez More on the bone-kidney axis--lessons from hypophosphataemia Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1521 - 1523. [Full Text] [PDF]

				S. Ferrari Single Gene Mutations and Variations Affecting Bone Turnover and Strength: a Selective 2006 Update IBMS BoneKEy, December 1, 2006; 3(12): 11 - 29. [Abstract] [Full Text] [PDF]

				D. M. Antoniucci, T. Yamashita, and A. A. Portale Dietary Phosphorus Regulates Serum Fibroblast Growth Factor-23 Concentrations in Healthy Men J. Clin. Endocrinol. Metab., August 1, 2006; 91(8): 3144 - 3149. [Abstract] [Full Text] [PDF]

				S. Liu, W. Tang, J. Zhou, J. R. Stubbs, Q. Luo, M. Pi, and L. D. Quarles Fibroblast Growth Factor 23 Is a Counter-Regulatory Phosphaturic Hormone for Vitamin D J. Am. Soc. Nephrol., May 1, 2006; 17(5): 1305 - 1315. [Abstract] [Full Text] [PDF]

				D. Rendina, G. Mossetti, G. De Filippo, M. Cioffi, and P. Strazzullo Fibroblast Growth Factor 23 Is Increased in Calcium Nephrolithiasis with Hypophosphatemia and Renal Phosphate Leak J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 959 - 963. [Abstract] [Full Text] [PDF]

				E. Schipani, A. Zallone, G. J. Strewler, J. W. Pike, S. Ferrari, Y. Jiang, and E. Seeman Meeting Report from the 27th Annual Meeting of the American Society for Bone and Mineral Research: September 23-27, 2005 in Nashville, Tennessee, USA IBMS BoneKEy, January 1, 2006; 3(1): 29 - 62. [Full Text] [PDF]

				X. Yu, O. A. Ibrahimi, R. Goetz, F. Zhang, S. I. Davis, H. J. Garringer, R. J. Linhardt, D. M. Ornitz, M. Mohammadi, and K. E. White Analysis of the Biochemical Mechanisms for the Endocrine Actions of Fibroblast Growth Factor-23 Endocrinology, November 1, 2005; 146(11): 4647 - 4656. [Abstract] [Full Text] [PDF]

				T. Larsson, S. I. Davis, H. J. Garringer, S. D. Mooney, M. S. Draman, M. J. Cullen, and K. E. White Fibroblast Growth Factor-23 Mutants Causing Familial Tumoral Calcinosis Are Differentially Processed Endocrinology, September 1, 2005; 146(9): 3883 - 3891. [Abstract] [Full Text] [PDF]

				M. Fukagawa and J. J. Kazama With or without the kidney: the role of FGF23 in CKD Nephrol. Dial. Transplant., July 1, 2005; 20(7): 1295 - 1298. [Full Text] [PDF]

				T. Berndt and R. Kumar The Phosphatonins and the Regulation of Phosphorus Homeostasis IBMS BoneKEy, June 1, 2005; 2(6): 5 - 16. [Full Text] [PDF]