| [ Summary ] |
The presence of a systemic factor regulating vitamin D metabolism has been postulated in tumor-induced osteomalacia (TIO) and was recently demonstrated by the cloning of FGF23 as a causative factor for TIO. FGF23 reduces serum concentrations of 1,25 (OH)2D by regulating vitamin D metabolizing key enzymes responsible for anabolism and catabolism of bioactive vitamin D metabolite, 1,25-dihydroxyvitamin D [1,25 (OH)2D]. FGF23 null mice lacked the negative regulation of 25-hydroxyvitamin D-1α-hydroxylase (1 α-OHase) by 1,25 (OH)2D. In addition, recent findings indicate that serum concentrations of FGF23 are also regulated by 1,25 (OH)2D. These findings strongly suggest that FGF23 is physiologically essential for the negative feedback regulation of 1 α-OHase by 1,25 (OH)2D. Since FGF23 is a key regulatory factor for phosphate metabolism on another front, the mutual regulatory system between FGF23 and 1,25 (OH)2D probably plays an important role as one of the underlying mechanisms constituting the cross-talk between phosphate and vitamin D metabolism. |