Epithelial calcium transporter expression in human duodenum

2001 ◽  
Vol 280 (2) ◽  
pp. G285-G290 ◽  
Author(s):  
Natalie F. Barley ◽  
Alison Howard ◽  
David O'Callaghan ◽  
Stephen Legon ◽  
Julian R. F. Walters
Keyword(s):  
Vitamin D ◽  
Calcium Channel ◽  
Calcium Absorption ◽  
Apical Membrane ◽  
Calcium Influx ◽  
Basolateral Membrane ◽  
Cdna Probe ◽  
Vitamin D Metabolites ◽  
Expression Of Genes ◽  
Calbindin D

Calcium absorption in intestine and kidney involves transport through the apical membrane, cytoplasm, and basolateral membrane of the epithelial cells. Apical membrane calcium influx channels have recently been described in rabbit (epithelial calcium channel, ECaC) and rat (calcium transport protein, CaT1). We amplified from human duodenum a 446-base partial cDNA probe (ECAC2) having a predicted amino acid similarity of 97% to rat CaT1. Duodenum, but not ileum, colon, or kidney, expressed a 3-kb transcript. A larger transcript was also found in placenta and pancreas, and a different, faint transcript was found in brain. In duodenal biopsies from 20 normal volunteers, expression varied considerably but was not significantly correlated with vitamin D metabolites. This signal correlated with calbindin-D9k ( r = 0.48, P< 0.05) and more strongly with the plasma membrane calcium ATPase PMCA1 ( r = 0.83, P < 0.001). These data show that although individual variations in calcium channel transcripts are not vitamin D dependent, expression of genes governing apical entry and basolateral extrusion are tightly linked. This may account for some of the unexplained variability in calcium absorption.

scholarly journals Intestinal Calcium Absorption and Serum Vitamin D Metabolites in Normal Subjects and Osteoporotic Patients

1979 ◽  
Vol 64 (3) ◽  
pp. 729-736 ◽  
Author(s):  
J. C. Gallagher ◽  
B. Lawrence Riggs ◽  
John Eisman ◽  
Alan Hamstra ◽  
Sara B. Arnaud ◽  
...  
Keyword(s):  
Vitamin D ◽  
Calcium Absorption ◽  
Serum Vitamin ◽  
Normal Subjects ◽  
Intestinal Calcium Absorption ◽  
Vitamin D Metabolites ◽  
Serum Vitamin D

The CDX2-site polymorphism in the vitamin D receptor gene and expression of genes for intestinal calcium absorption

2003 ◽  
Vol 124 (4) ◽  
pp. A126
Author(s):  
Julian R. Walters ◽  
Mohammed Khanji ◽  
Natalie Barley ◽  
Orli Rhodes-Kendler ◽  
Umma Khair
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Receptor Gene ◽  
Intestinal Calcium Absorption ◽  
Vitamin D Receptor Gene ◽  
Expression Of Genes

Calcium Malabsorption in Elderly Women with Vertebral Fractures: Evidence for Resistance to the Action of Vitamin D Metabolites on the Bowel

1984 ◽  
Vol 66 (1) ◽  
pp. 103-107 ◽  
Author(s):  
R. M. Francis ◽  
M. Peacock ◽  
G. A. Taylor ◽  
J. H. Storer ◽  
B. E. C. Nordin
Keyword(s):  
Vitamin D ◽  
Vertebral Fractures ◽  
Calcium Absorption ◽  
Elderly Women ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Significant Difference ◽  
Before And After ◽  
Calcium Malabsorption

1. Radio-calcium absorption, plasma 25-hydroxyvitamin D [25-(OH)D] and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in 19 elderly women with, and 21 without, vertebral fractures, before and after treatment with 25-hydroxyvitamin D3 [25-(OH)D3], to establish whether malabsorption of calcium in elderly women with vertebral fractures has a cause different from that in elderly women without vertebral fractures. 2. Malabsorption of calcium and low plasma 25-(OH)D and 1,25-(OH)2D concentrations were common in both groups of women but there was no significant difference in these variables between the two groups. 3. After treatment with 40 μg of 25-(OH)D3 daily for 7 days, there was a significant increase in plasma 25-(OH)D and 1,25-(OH)2D in both groups of women, but radio-calcium absorption increased significantly only in the group without vertebral fractures. 4. Elderly women with vertebral fractures have malabsorption of calcium which is resistant to the action of vitamin D metabolites at concentrations which correct calcium malabsorption in elderly women without vertebral fractures.

scholarly journals Pregnancy Up-Regulates Intestinal Calcium Absorption and Skeletal Mineralization Independently of the Vitamin D Receptor

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 886-895 ◽  
Author(s):  
Neva J. Fudge ◽  
Christopher S. Kovacs
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Fold Increase ◽  
Normal Diet ◽  
Intestinal Calcium Absorption ◽  
A Genome ◽  
Pregnancy And Lactation ◽  
Turnover Markers ◽  
Calbindin D

Without the vitamin D receptor (VDR), adult mammals develop reduced intestinal calcium absorption, rickets, and osteomalacia. Intestinal calcium absorption normally increases during pregnancy so that the mother can supply sufficient calcium to her fetuses. The maternal skeleton is rapidly resorbed during lactation to provide calcium needed for milk; that lost bone mineral content (BMC) is completely restored after weaning. We studied Vdr null mice to determine whether these adaptations during pregnancy and lactation require the VDR. Vdr nulls were severely rachitic at 10 wk of age on a normal diet. Pregnancy induced a 158% increase in Vdr null BMC to equal the pregnant wild-type (WT) value. Lactation caused BMC losses that were equal in Vdr nulls and WT. Vdr nulls recovered after weaning to a BMC 50% higher than before pregnancy and equal to WT. Additional analyses showed that during pregnancy, duodenal 45Ca absorption increased in Vdr nulls, secondary hyperparathyroidism lessened, bone turnover markers decreased, and osteoid became fully mineralized. A genome-wide microarray analysis of duodenal RNA found marked reduction of Trpv6 in Vdr nulls at baseline but a 13.5-fold increase during pregnancy. Calbindin D-9K (S100g) and Ca2+-ATPase (Pmca1) were not altered by pregnancy. Several other solute transporters increased during pregnancy in Vdr nulls. In summary, Vdr nulls adapt to pregnancy by up-regulating duodenal Trpv6 and intestinal 45Ca absorption, thereby enabling rapid normalization of BMC during pregnancy. These mice lactate normally and fully restore BMC after weaning. Therefore, VDR is not required for the skeletal adaptations during pregnancy, lactation, and after weaning.

Effects of 1,25(OH)2D3 and calcium channel blockers on cecal calcium transport in the rat

1985 ◽  
Vol 248 (6) ◽  
pp. G676-G681 ◽  
Author(s):  
M. J. Favus ◽  
E. Angeid-Backman
Keyword(s):  
Vitamin D ◽  
Calcium Channel ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Channel Blockers ◽  
Dihydroxyvitamin D3 ◽  
High Concentrations ◽  
Absorptive Flux ◽  
Mucosal Side

To determine whether calcium transport across rat cecum is vitamin D dependent, we measured in vitro bidirectional calcium fluxes under short-circuited conditions across cecum from rats that were vitamin D deficient, vitamin D replete, or vitamin D deficient or vitamin D replete and injected with either 10, 25, or 75 ng of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] daily for 4 days before study. Vitamin D deficiency decreased net calcium absorption (Jnet) by reducing the mucosal-to-serosal absorptive flux (Jm----s) from 168 +/- 18 to 33 +/- 5 nmol X cm-2 X h-1 (mean +/- SE, P less than 0.0001). Twenty-five nanograms of 1,25(OH)2D3 raised Jm----s to 124 +/- 17 nmol X cm-2 X h-1, not different from values in vitamin D-replete rats. Although active calcium absorption by cecum appears to respond to vitamin D, calcium Jm----s is near maximal under normal conditions, and further stimulation follows only pharmacological doses of 1,25(OH)2D3. The in vitro addition of the calcium channel blocker verapamil (5 X 10(-5) M) to the mucosal side of cecum from vitamin D-replete rats reduced calcium Jm----s, but lower concentrations of verapamil or nitrendipine (10(-5) to 10(-9) M) did not reduce calcium Jm----s. The lack of inhibition by low concentrations of channel blockers suggest that the plasma membrane channels for calcium translocation across intestinal epithelium may not be analogous to voltage-dependent calcium channels in excitable tissue. The inhibition of cecal calcium transport that was blocked by high concentrations of verapamil may represent a nonspecific effect of the agent.

The effects of Vitamin D metabolites on expression of genes for calcium transporters in human duodenum

2007 ◽  
Vol 103 (3-5) ◽  
pp. 509-512 ◽  
Author(s):  
Julian R.F. Walters ◽  
Sara Balesaria ◽  
Umma Khair ◽  
Sonia Sangha ◽  
Linda Banks ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Metabolites ◽  
Expression Of Genes

scholarly journals Calcium influx in induced differentiation of murine erythroleukemia cells

Blood ◽  
1993 ◽  
Vol 81 (3) ◽  
pp. 783-792 ◽  
Author(s):  
B Gillo ◽  
YS Ma ◽  
AR Marks
Keyword(s):  
Calcium Channel ◽  
Calcium Influx ◽  
Cdna Probe ◽  
Erythroid Differentiation ◽  
Early Event ◽  
Induced Differentiation ◽  
Erythroleukemia Cells ◽  
Murine Erythroleukemia ◽  
Murine Erythroleukemia Cells

Abstract Murine erythroleukemia cells (MELC) have served as a model for examining the regulation of erythroid differentiation. However, the role of Ca2+ in the signal transduction pathways regulating differentiation remains unclear. To begin to address this uncertainty we have characterized the regulation of cytoplasmic Ca2+ and the possible role of calcium channels during induced differentiation in MELC. MELC can be induced to terminal differentiation using the polar/apolar compound hexamethylene bisacetamide (HMBA). We found that HMBA stimulated Ca2+ influx within 3 to 6 minutes and that Ca2+ entry was required but not sufficient for MELC growth and differentiation. Nifedipine (1 to 10 mumol/L), a calcium channel antagonist, blocked HMBA-induced Ca2+ influx and inhibited differentiation by approximately 60%. Depolarization of the MELC membrane did not induce Ca2+ influx and whole-cell patch-clamp recordings failed to detect a voltage-activated Ca2+ current, suggesting that MELC do not express detectable levels of a functional voltage-dependent calcium channel (VDCC). However, a cDNA probe encoding a portion of the alpha 1 subunit of the cardiac VDCC detected an approximately 8-kb mRNA on Northern blots of total MELC RNA. Taken together, these data show that Ca2+ influx is an early event associated with HMBA-induced differentiation in MELC, blockade of this calcium influx inhibits induced differentiation, and a voltage- insensitive dihydropyridine-sensitive calcium channel may be involved in Ca2+ influx in MELC.

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