Interactions between FGF23 and vitamin D

Fibroblast growth factor-23 (FGF23) controls the homeostasis of both phosphate and vitamin D. Bone-derived FGF23 can suppress the transcription of 1 alpha-hydroxylase (1 alpha(OH)ase) to reduce renal activation of vitamin D (1,25(OH)(2)D-3). FGF23 can also activate the transcription of 24-hydroxylase to enhance the renal degradation process of vitamin D. There is a counter-regulation for FGF23 and vitamin D; 1,25(OH)(2)D-3 induces the skeletal synthesis and the release of FGF23, while FGF23 can suppress the production of 1,25(OH)(2)D-3 by inhibiting 1 alpha(OH)ase synthesis. Genetically ablating FGF23 activities in mice resulted in higher levels of renal 1 alpha(OH)ase, which is also reflected in an increased level of serum 1,25(OH)(2)D-3, while genetically ablating 1 alpha(OH)ase activities in mice reduced the serum levels of FGF23. Similar feedback control of FGF23 and vitamin D is also detected in various human diseases. Further studies are required to understand the subcellular molecular regulation of FGF23 and vitamin D in health and disease.

Automated summary

FGF23 controls the homeostasis of phosphate and vitamin D by suppressing the activation of vitamin D and enhancing its degradation process. There is a counter-regulation between FGF23 and vitamin D, with FGF23 inhibiting the synthesis of 1 alpha-hydroxylase (1 alpha(OH)ase) which produces vitamin D, while vitamin D induces the synthesis and release of FGF23. This feedback control is also observed in various human diseases.