Phosphate-sensing and regulatory mechanism of FGF23 production.

Journal of Endocrinological Investigation
Yuichi Takashi, Seiji Fukumoto

Abstract

Inorganic phosphate (Pi) is an essential mineral for human. Hypophosphatemia and hyperphosphatemia cause rickets/osteomalacia and ectopic calcification, respectively, indicating that serum Pi level needs to be regulated. Fibroblast growth factor (FGF) 23 is a principal hormone to regulate serum Pi level. FGF23 is produced by the bone, especially by the osteoblasts and osteocytes, and works by binding to FGF receptor (FGFR) 1c and α-Klotho complex in the kidney. FGF23 reduces serum Pi level by inhibiting both renal phosphate reabsorption and intestinal phosphate absorption via reduction of serum 1,25-dihydroxyvitamin D level. It has been unclear how the bone senses changes of serum Pi level and how the bone regulates the production of FGF23. Our recent results indicate that the post-translational modification of FGF23 protein through a gene product of GALNT3 is the main regulatory mechanism of enhanced FGF23 production by high dietary Pi. Furthermore, high extracellular Pi directly activates FGFR1 and its downstream intracellular signaling pathway regulates the expression level of GALNT3. We propose that FGFR1 works as a Pi-sensing receptor in the regulation of FGF23 production and serum Pi level. There is a negative feedback sy...Continue Reading

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Citations

Sep 29, 2020·Frontiers in Endocrinology·Rafiou AgoroKenneth E White
Oct 4, 2020·Nutrients·Juan Serna, Clemens Bergwitz
Aug 12, 2020·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Michael Pazianas, Paul D Miller
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