The experimentally determined rate of transcellular calcium transport in the duodenum of vitamin D-replete: rats is nearly two orders of magnitude greater than expected from the rate of self-diffusion of the calcium ion in the cytosol. No transcellular calcium transport occurs in vitamin D-deficient animals. The excess diffusional flux can be explained by the presence in the duodenal mucosal cells of calbindin D-9k, a vitamin D-dependent cytosolic protein that binds two calcium ions per molecule, thereby increasing the cytosolic concentration of diffusible calcium. The relationship between the V-max of transport and calbindin D-9k concentration is positive and linear, both in the steady state and after vitamin D administration, and is abolished on vitamin D deficiency. Transport and calbindin content are upregulated. by a low calcium diet and downregulated. by a high calcium diet. In contrast, the paracellular pathway is non-saturable and directly proportional to the luminal calcium ion concentration. Thus, the rate of calcium transport across the intestinal cell is essentially determined by the rate of calcium movement through the cytosol, catalyzed by the cytosolic calcium binding protein, calbindin D-9k, rather than by membrane transport. An intracellular binding protein is likely to be the molecular mechanism when the transcellular movement oi an ion exceeds its self-diffusion rate. Copyright (C) 1996 Elsevier Science Inc.
