Abstract

Whole-body calcium metabolism is controlled by actions occurring within and between a number of tissues including the intestine, kidney, bone, fat mass, and brain in an effort to maintain serum calcium within a narrow range. In this light, intestinal calcium absorption from the diet is an essential process maintaining calcium balance and bone health. Under normal conditions, the saturable portion of intestinal phosphate absorption is dependent upon adequate vitamin D status. However, the mechanism for that regulation is not clear. The central player in phosphate absorption is the apical membrane sodium–phosphate cotransporter, NaPi IIb. However, while vitamin D changes the level of the NaPi Iib protein at the membrane, it does not strongly regulate the NaPi IIb gene and if it does so at all, it appears to be indirectly through an as yet unidentified factor. More importantly, even though both serum 1,25(OH)2D and intestinal phosphate absorption increase during dietary phosphate restriction, the body still has the ability to adapt to low-phosphate diets even in the absence of vitamin D receptor (VDR) or CYP27B1. This suggests that a major regulator of phosphate absorption is vitamin-D-independent and that there are critical regulators of intestinal phosphate absorption that have yet to be discovered.

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