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2015 ; 21
(23
): 7142-54
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Molecular aspects of intestinal calcium absorption
#MMPMID26109800
Diaz de Barboza G
; Guizzardi S
; Tolosa de Talamoni N
World J Gastroenterol
2015[Jun]; 21
(23
): 7142-54
PMID26109800
show ga
Intestinal Ca(2+) absorption is a crucial physiological process for maintaining
bone mineralization and Ca(2+) homeostasis. It occurs through the transcellular
and paracellular pathways. The first route comprises 3 steps: the entrance of
Ca(2+) across the brush border membranes (BBM) of enterocytes through epithelial
Ca(2+) channels TRPV6, TRPV5, and Cav1.3; Ca(2+) movement from the BBM to the
basolateral membranes by binding proteins with high Ca(2+) affinity (such as
CB9k); and Ca(2+) extrusion into the blood. Plasma membrane Ca(2+) ATPase
(PMCA1b) and sodium calcium exchanger (NCX1) are mainly involved in the exit of
Ca(2+) from enterocytes. A novel molecule, the 4.1R protein, seems to be a
partner of PMCA1b, since both molecules co-localize and interact. The
paracellular pathway consists of Ca(2+) transport through transmembrane proteins
of tight junction structures, such as claudins 2, 12, and 15. There is evidence
of crosstalk between the transcellular and paracellular pathways in intestinal
Ca(2+) transport. When intestinal oxidative stress is triggered, there is a
decrease in the expression of several molecules of both pathways that inhibit
intestinal Ca(2+) absorption. Normalization of redox status in the intestine with
drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal
Ca(2+) transport to control values. Calcitriol [1,25(OH)?D?] is the major
controlling hormone of intestinal Ca(2+) transport. It increases the gene and
protein expression of most of the molecules involved in both pathways. PTH,
thyroid hormones, estrogens, prolactin, growth hormone, and glucocorticoids
apparently also regulate Ca(2+) transport by direct action, indirect mechanism
mediated by the increase of renal 1,25(OH)?D? production, or both. Different
physiological conditions, such as growth, pregnancy, lactation, and aging, adjust
intestinal Ca(2+) absorption according to Ca(2+) demands. Better knowledge of the
molecular details of intestinal Ca(2+) absorption could lead to the development
of nutritional and medical strategies for optimizing the efficiency of intestinal
Ca(2+) absorption and preventing osteoporosis and other pathologies related to
Ca(2+) metabolism.
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