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Parathyroid Hormone Regulates Fibroblast Growth Factor-23 in a Mouse Model of Primary Hyperparathyroidism

Takehisa Kawata^*, Yasuo Imanishi^*, Keisuke Kobayashi^*, Takami Miki, Andrew Arnold, Masaaki Inaba^* and Yoshiki Nishizawa^*

Departments of ^* Metabolism, Endocrinology and Molecular Medicine and Geriatrics and Neurology, Osaka City University Graduate School of Medicine, Osaka, Japan; and Center for Molecular Medicine, University of Connecticut School of Medicine, Farmington, Connecticut

Correspondence: Dr. Yasuo Imanishi, Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Phone: +81-6-6645-3806; Fax: +81-6-6645-3808; E-mail: imanishi{at}med.osaka-cu.ac.jp

Received for publication July 26, 2006. Accepted for publication May 31, 2007.

The importance of fibroblast growth factor 23 (FGF-23) in the pathogenesis of phosphate wasting disorders has been established, but controversy remains about how parathyroid hormone (PTH), which also stimulates urinary phosphate excretion, regulates the circulating level of FGF-23. We found that the serum FGF-23 concentration was higher in PTH-cyclin D1 transgenic mice, a model of primary hyperparathyroidism, than in wild-type mice. The serum FGF-23 concentration was significantly and directly correlated with serum PTH and calcium, and inversely correlated with phosphate levels in 90- to 118-week-old mice (all P < 0.005). Quantitative real-time reverse-transcriptase PCR revealed abundant expression of fgf23 in bone, especially in calvaria. The fgf23 expression in calvaria was significantly higher in the transgenic mice compared to the wild-type mice, and correlated well with serum FGF-23 levels. There was a direct correlation between the expression of fgf23 and the expression of osteocalcin and ALP, suggesting that activation of osteoblasts is important in the regulation of FGF-23. Serum FGF-23 levels decreased in the transgenic mice after parathyroidectomy. In conclusion, PTH plays a major role in the regulation of serum FGF-23 level in primary hyperparathyroidism, likely via activation of osteoblasts in bone.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673