On the Molecular Mechanism of Intestinal Calcium Transport

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Abstract
The calcium concentration in blood, presumably similar to the calcium concentration in ancient seas during evolution, is a relatively stable biological “constant”, averaging about 2.5 mM (10 mg/dl) in the normal individual. The maintenance of blood calcium concentrations is primarily the function of the calcium regulating hormones, namely, parathyroid hormone (PTH), calcitonin and the vitamin D hormone, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) (Bronner & Coburn, 1982; Lawson, 1978). The main organ systems involved in systemic calcium homeostasis are the intestine, kidney and skeleton. Parathyroid hormone, secreted during periods of hypocalcemia, exerts three main effects: (a) increases bone resorption, (b) decreases phosphate reabsorption by renal tubules and (c) stimulates the synthesis of l,25(OH)2D3 by the renal 25(OH)D3–1-hydroxylase system. The vitamin D hormone: (a) synergizing with parathyroid hormone, increases the bone resorptive process, (b) increases the intestinal absorption of calcium, and (c) increases the reabsorption of calcium by the distal renal tubules (Figure 1). The net effect of the dual action of parathyroid hormone and 1,25(OH)2D3 is to assure that normal levels of blood Ca2+ are maintained. Phosphate absorption by the intestine is also stimulated by vitamin D and 1,25(OH)2D3 (Wasserman & Taylor, 1973; Peterlik & Wasserman, 1978). Calcitonin, on the other hand, is secreted during periods of hypercalcemia and, by inhibiting osteoclastic bone resorption, brings blood Ca2+ levels down to within the normal range (Mac Intyre, 1986).