Schematic view of vitamin D (VD) signaling pathway mediated VD receptor (VDR). Active form of VD is biosynthesized from precursors taken from diet as well as endogenously generated cholesterol metabolites, and catabolized by P450 enzymes depicted in the figure. The key conversion into the active form of VD is conducted by cytochrome P450 (CYP)27B1, and the major catabolizing enzyme is CYP24A1. Active form of VD exerts biological action through gene regulation operated by VDR. Genetic mutations deficient of CYP27B1 and VDR function are causal hereditary rickets, similar to rachitic abnormality seen in rickets by nutritious deficiency of VD. Organs related with VD action are illustrated. UVB, ultraviolet B; 25(OH)D3, 25-hydroxy-vitamin D3; FGF23, fibroblast growth factor 23; PTH, parathyroid hormone; VDDR, vitamin D-dependent rickets; RXR, retinoid X receptor; VDR, vitamin D receptor; VDRE, vitamin D response element
