Calcemic actions of vitamin D: Effects on the intestine, kidney and bone

The analysis of mice that lack systemically the actions of the active form of vitamin D, 1,25(OH)2D, has shown that 1,25(OH)2D is an essential regulator of calcium homeostasis and that its actions are aimed at maintaining serum calcium levels within narrow limits. Especially the stimulation of intestinal calcium transport by 1,25(OH)2D is important for calcium and bone homeostasis. The involved transporters are however still elusive. The targeted deletion of 1,25(OH)2D action in chondrocytes has provided compelling evidence for a paracrine control of bone development and endocrine regulation of phosphate homeostasis by 1,25(OH)2D. Targeting vitamin D receptor (VDR) function in other tissues will further enhance our understanding of the cell-type specific action of 1,25(OH)2D. In this review, we will discuss the current understanding and remaining questions concerning the calcemic actions of 1,25(OH)2D in the intestine, kidney and bone, with special focus on the evidence obtained by the use of transgenic mouse models.