Intestinal calcium transport: the cellular pathway.

The active calcium transport process in the intestine is transcellular. Entry across the brush border of the enterocyte is down an electrochemical gradient, probably via calcium channels. The entry process, although modified by vitamin D, does not appear to be the rate-limiting step, as total vitamin D deficiency lowers the rate of entry only by about a third, whereas active calcium transport is wholly inhibited. Calcium extrusion is effected by the Ca-ATPase, is against an electrochemical gradient, and requires a supply of energy. However, it is not the rate-limiting step, as extrusion capacity is more than sufficient to handle the maximum transcellular flux of calcium. It is the flow of calcium inside the cell, from the brush-border pole to the pump at the basolateral side, that is rate-limiting. Basal calcium flow, in the absence of the cytosolic, vitamin D-dependent calcium-binding protein, CaBP, is only about 1/70 of the maximum rate, Vm, in the vitamin D-replete duodenum. CaBP levels vary linearly with the Vm. Moreover, interference with calcium binding by CaBP interferes with active calcium transport. Active calcium transport is totally regulated by vitamin D or processes that modify the action or metabolism of the sterol. Since, however, active calcium transport is only one of the two routes of calcium absorption, the other being a passive, paracellular process, up- or down-regulation of active transport may have only a limited effect on total calcium absorption.