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  • Title: [Intestinal absorption of calcium and its regulation. Tissue, membrane and molecular events].
    Author: Pansu D, Bellaton C, Roche C.
    Journal: Diabete Metab; 1984 May; 10(2):106-20. PubMed ID: 6378683.
    Abstract:
    The intestinal absorption of calcium involves an active transport against an electrochemical gradient, a saturable and a nonsaturable transfer following the gradient. The active and the saturable components are transcellular, the nonsaturable component is partly paracellular. Calcium transfer through the intestinal cell includes three steps: 1) the "down-hill" crossing of the brush-border implies binding to specific sites, carrier-mediated transport using channels or carrier proteins specific to Ca and dependent upon composition phosphorylations alkaline phosphatases; the phospholipid composition of the brush-border also plays a role; 2) the intracellular transfer is characterized by an uptake by such organelles as mitochondria, lysosomes and Golgi vesicles and by a transfer on a specific calcium-binding protein; 3) the "up-hill" transfer across the baso-lateral membrane requires energy and energy is mediated by an ATP-activated Ca2+ pump and a Na+/Ca2+ antiport. 1.25 dihydroxycholecalciferol, steroid hormone synthetized from vitamin D3 is the major direct regulator of Ca absorption: in the vitamin D-deprived animal, it increases the selective permeability for Ca of the brush-border, induces the synthesis of proteins after genomic transcription, activates the Ca-ATPases, and acts as a trophic hormone. The other hormones principally act by modulation of the renal biosynthesis of 1.25 dihydroxycholecalciferol. The efficiency of Ca absorption depends on site, with duodenum greater than jejunum greater than caecum greater than ileum. Dietary constituents such as carbohydrates and amino acids increase Ca absorption whereas phytic acid and excess of phosphorus decrease it. They act by modifying Ca bioavailability and perhaps brush-border permeability. Adaptation to increased demand occurs during growth, pregnancy and lactation in normal states but disappears during vitamin D deficiency. In man, lowered efficiency with increasing age is often aggravated by a low calcium diet.
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