Figure 1: The synthesis and metabolism of vitamin D in the regulation of mineral homeostasis and nonskeletal functions. When under exposed to solar UVB (ultraviolet B), 7-dehydrocholesterol in the skin is converted to previtamin , which is immediately converted to vitamin D3. Vitamin D can also be obtained from dietary vitamin and incorporated into chylomicrons. Vitamin D in the circulation is bound to DBP (vitamin D-binding protein), which transports it to the liver where it is converted to 25-hydroxyvitamin D by vitamin D-25-hydroxylase. The biologically inactive 25-hydroxyvitamin D must be converted in the kidneys to active 1,25-hydroxyvitamin D by 1-OHase (25-hydroxyvitamin 1α-hydroxylase). Serum PTH (parathyroid hormone), low phosphorus/calcium, sex hormones, calcitonin, and prolactin can increase (⊕) the renal production of 1,25-hydroxyvitamin D. However, FGF-23 (fibroblast growth factor 23) and 1,25-hydroxyvitamin D have feedback functions to inhibit (⊝) 1-OHase. Finally, the active 1,25-hydroxyvitamin D can bind to VDR-RXR (vitamin D receptor-retinoic acid x-receptor complex) in the intestine, bone, and parathyroid glands and then exert the classical function of mineral homeostasis. In addition, it also has nonskeletal functions when bound to VDR-RXR in other organs (breast, colon, prostate, kidney, pancreas) or immune cells (macrophages/monocytes). FGFR: FGF-23 receptor; TRPV6: transient receptor potential cation channel, subfamily V, member 6; RANKL: receptor activator of nuclear factor-κB ligand; RANK: the receptor for RANKL on preosteoclasts.