2013
DOI: 10.4103/2230-8210.117187
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The intestinal calcistat: Determinant of clinical vitamin D deficiency

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Cited by 6 publications
(5 citation statements)
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“…[ 4 5 7 ] After excluding the possibility of co-existing non-PTH mediated hypercalcemia, a number of theories have been proposed to explain this functional hypoparathyroidism. They include redefining the upper normal limits of PTH levels in the normal population,[ 8 ] intestinal calcium absorption adaptation theory (intestinal calcistat),[ 9 10 11 ] circadian variations in PTH,[ 12 ] magnesium (Mg) deficiency[ 13 ] and lastly the variations in Vitamin D binding protein among population[ 14 ] and its impact on the free Vitamin D levels.…”
Section: Introductionmentioning
confidence: 99%
“…[ 4 5 7 ] After excluding the possibility of co-existing non-PTH mediated hypercalcemia, a number of theories have been proposed to explain this functional hypoparathyroidism. They include redefining the upper normal limits of PTH levels in the normal population,[ 8 ] intestinal calcium absorption adaptation theory (intestinal calcistat),[ 9 10 11 ] circadian variations in PTH,[ 12 ] magnesium (Mg) deficiency[ 13 ] and lastly the variations in Vitamin D binding protein among population[ 14 ] and its impact on the free Vitamin D levels.…”
Section: Introductionmentioning
confidence: 99%
“…According to our immunohistochemistry results, it showed that positive staining in the apical membranes of both small intestine and colon, suggesting pCaSR is mainly expressed in the apical membranes of pig villus cells. An early study mirrored this result given that it claimed that CaSR appeared on the brush border of the intestine (Garg et al, 2013). However, it is difficult to determine which specific cells express pCaSR by using immunohistochemical staining.…”
Section: Discussionmentioning
confidence: 86%
“…[9] This suggests that it is the calcium absorptive mechanism, rather than dietary calcium intake, will decide the adequacy of calcium homeostasis. An alternative hypothesis has been proposed, wherein the adaptation of calcium absorption occurs at the level of intestine called “intestinal calcistat.”[1011] This “calcistat” senses the calcium intake or available calcium in the gastrointestinal (GI) tract and regulates the generation of active Vitamin D in intestinal cells to adjust FCA. With daily calcium intake of <500 mg, the FCA is about 60%–80%, which can easily supply the daily needs of calcium, i.e., 200 mg.…”
Section: Why – Calcium Supplementation?mentioning
confidence: 99%