Vitamin D and Magnesium Absorption in Man

1979 ◽  
Vol 57 (1) ◽  
pp. 121-123 ◽  
Author(s):  
A. Hodgkinson ◽  
D. H. Marshall ◽  
B. E. C. Nordin
Keyword(s):  
Vitamin D ◽  
Calcium Transport ◽  
Alkaline Earth ◽  
Calcium Balance ◽  
Slight Effect ◽  
Strontium Barium ◽  
Active Calcium ◽  
The Mean ◽  
Calcium And Magnesium ◽  
Stimulation Of

1. The effects of vitamin D and its hydroxylated derivatives on calcium and magnesium absorption have been examined in 47 balance studies on patients with various disorders of calcium or bone metabolism. 2. Vitamin D significantly increased the mean net absorption of calcium and also the calcium balance. The mean net absorption of magnesium was also significantly increased although the rise was much less than that of calcium and the mean magnesium balance was unaffected. 3. It is suggested that the slight effect of vitamin D on magnesium absorption may be incidental to its stimulation of active calcium transport, since the latter system has weak affinities for other alkaline earth ions including strontium, barium and magnesium.

scholarly journals Analysis of 1,25-Dihydroxyvitamin D3 Genomic Action Reveals Calcium-Regulating and Calcium-Independent Effects in Mouse Intestine and Human Enteroids

2020 ◽  
Vol 41 (1) ◽  
pp. e00372-20
Author(s):  
Shanshan Li ◽  
Jessica De La Cruz ◽  
Steven Hutchens ◽  
Somshuvra Mukhopadhyay ◽  
Zachary K. Criss ◽  
...  
Keyword(s):  
Vitamin D ◽  
Calcium Transport ◽  
Target Genes ◽  
Dihydroxyvitamin D3 ◽  
Transgenic Expression ◽  
Distal Intestine ◽  
Dihydroxyvitamin D ◽  
Active Calcium ◽  
Independent Effects ◽  
Proximal Intestine

ABSTRACTAlthough vitamin D is critical for the function of the intestine, most studies have focused on the duodenum. We show that transgenic expression of the vitamin D receptor (VDR) only in the distal intestine of VDR null mice (KO/TG mice) results in the normalization of serum calcium and rescue of rickets. Although it had been suggested that calcium transport in the distal intestine involves a paracellular process, we found that the 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]-activated genes in the proximal intestine associated with active calcium transport (Trpv6, S100g, and Atp2b1) are also induced by 1,25(OH)2D3 in the distal intestine of KO/TG mice. In addition, Slc30a10, encoding a manganese efflux transporter, was one of the genes most induced by 1,25(OH)2D3 in both proximal and distal intestine. Both villus and crypt were found to express Vdr and VDR target genes. RNA sequence (RNA-seq) analysis of human enteroids indicated that the effects of 1,25(OH)2D3 observed in mice are conserved in humans. Using Slc30a10−/− mice, a loss of cortical bone and a marked decrease in S100g and Trpv6 in the intestine was observed. Our findings suggest an interrelationship between vitamin D and intestinal Mn efflux and indicate the importance of distal intestinal segments to vitamin D action.

Calcium transport in small intestine during pregnancy and lactation

1980 ◽  
Vol 239 (1) ◽  
pp. E64-E68 ◽  
Author(s):  
B. P. Halloran ◽  
H. F. DeLuca
Keyword(s):  
Vitamin D ◽  
Reproductive Cycle ◽  
Calcium Transport ◽  
Plasma Concentrations ◽  
Dihydroxyvitamin D ◽  
Control Value ◽  
1,25 Dihydroxyvitamin D ◽  
Everted Gut Sac ◽  
Pregnancy And Lactation ◽  
Active Calcium

The factors involved in calcium homeostasis during the mammalian reproductive cycle and specifically in the control of active calcium transport in the intestine have not been thoroughly investigated. For this reason calcium transport in the intestine was measured in vitamin D-replete and vitamin D-deficient rats during pregnancy and lactation using the everted gut sac technique. In addition the changes in the plasma concentrations of calcium and 1,25-dihydroxyvitamin D were measured and correlated with transport. During the later stages of pregnancy and during lactation, the concentration of calcium in the plasma is reduced 10-30%. In turn, in the vitamin D-replete rat, the concentration of 1,25-dihydroxyvitamin D in the plasma increases from a control value of 26 pg/ml to 158 pg/ml at day 14 of lactation. Calcium transport in the intestine increases late in pregnancy, peaks during lactation, and then falls to control values by 3 wk postweaning in both vitamin D-replete and D-deficient animals. These findings strengthen the established relationship between 1,25-dihydroxyvitamin D and active calcium transport in the intestine as well as suggest that some factor(s) independent of vitamin D is stimulating intestinal calcium transport during the reproductive cycle.

Chronic metabolic acidosis stimulated transcellular and solvent drag-induced calcium transport in the duodenum of female rats

2006 ◽  
Vol 291 (3) ◽  
pp. G446-G455 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Kukiat Tudpor ◽  
Naritsara Pulsook ◽  
Nateetip Krishnamra
Keyword(s):  
Metabolic Acidosis ◽  
Tight Junction ◽  
Mrna Expression ◽  
Calcium Transport ◽  
Female Rats ◽  
Calcium Balance ◽  
Solvent Drag ◽  
Chronic Metabolic Acidosis ◽  
Active Calcium ◽  
Relative Mrna Expression

Chronic metabolic acidosis results in a negative calcium balance as a result of bone resorption and renal calcium loss. However, reports on the changes in intestinal calcium transport have been controversial. The present investigation therefore aimed to study the effects of chronic metabolic acidosis induced by 1.5% NH4Cl administration on the three components of duodenal calcium transport, namely, solvent drag-induced, transcellular active, and passive paracellular components, in rats using an in vitro Ussing chamber technique. The relative mRNA expression of genes related to duodenal calcium transport was also determined. We found that 21-day chronic metabolic acidosis stimulated solvent drag-induced and transcellular active duodenal calcium transport but not passive paracellular calcium transport. Our results further demonstrated that an acute direct exposure to serosal acidic pH, in contrast, decreased solvent drag-induced calcium transport in a pH-dependent fashion but had no effect on transcellular active calcium transport. Neither the transepithelial resistance nor duodenal permeability to Na+, Cl−, and Ca2+ via the passive paracellular pathway were altered by chronic metabolic acidosis, suggesting that widening of the tight junction and changes in the charge-selective property of the tight junction did not occur. Thus the enhanced duodenal calcium transport observed in chronic metabolic acidosis could have resulted from a long-term adaptation, possibly at the molecular level. RT-PCR study revealed that chronic metabolic acidosis significantly increased the relative mRNA expression of duodenal genes associated with solvent drag-induced transport, i.e., the β1-subunit of Na+-K+-ATPase, zonula occludens-1, occludin, and claudin-3, and with transcellular active transport, i.e., transient receptor potential vanilloid family Ca2+ channels 5 and 6 and plasma membrane Ca2+-ATPase isoform 1b. Total plasma calcium and free ionized calcium and magnesium concentrations were also increased, whereas serum parathyroid hormone and 1α,25-dihydroxyvitamin D3 levels were not changed. The results indicated that 21-day chronic metabolic acidosis affected the calcium metabolism in rats partly through enhancing the mRNA expression of crucial duodenal genes involved in calcium absorption, thereby stimulating solvent drag-induced and transcellular active calcium transport in the duodenum.

Localization of vitamin D-dependent active Ca2+ transport in rat duodenum and relation to CaBP

1986 ◽  
Vol 251 (3) ◽  
pp. G314-G320 ◽  
Author(s):  
C. Roche ◽  
C. Bellaton ◽  
D. Pansu ◽  
A. Miller ◽  
F. Bronner
Keyword(s):  
Vitamin D ◽  
Brush Border ◽  
Calcium Binding ◽  
Calcium Transport ◽  
Positive Function ◽  
Extrusion Process ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Rat Duodenum ◽  
Active Calcium

Vitamin D-replete (+D) and vitamin D-deficient (-D) rats received by intraperitoneal injection varying amounts of 1,25-dihydroxyvitamin D3, and 4 h (+D) or 9 h (-D) later everted duodenal sacs were prepared to evaluate active calcium transport, i.e., the amount of calcium found in the serosal fluid. At the same time, duodenal calcium-binding protein (CaBP) content was measured. Calcium transport was a close positive function of CaBP content. It was not detectable when CaBP content was zero and increased linearly without plateauing as CaBP content increased to 100 nmol calcium bound/g mucosa. Trifluoperazine (TFP) inhibited active calcium transport in a concentration-dependent manner. Experiments using vesicles prepared from brush-border or basolateral membranes indicated that TFP inhibited the calcium-extrusion process, with virtually no effect on calcium entry. It is concluded that vitamin D exerts its major regulation of active calcium transport in the rat duodenum via CaBP on transport steps beyond brush-border entry.

scholarly journals Stimulation of intestinal calcium-binding-protein mRNA synthesis in the nucleus of vitamin D-deficient chicks by 1,25-dihydroxycholecalciferol

1978 ◽  
Vol 175 (3) ◽  
pp. 1089-1094 ◽  
Author(s):  
R. Spencer ◽  
M. Charman ◽  
D. E. M. Lawson
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Free System ◽  
Rna Molecules ◽  
Pulse Dose ◽  
A Cell ◽  
Active Calcium ◽  
Stimulation Of

Stimulation of intestinal calcium transport by the hormone 1,25-dihydroxycholecalciferol appears to involve RNA transcriptions and the synthesis of new proteins. Although one of these proteins has been identified as calcium-binding protein, no RNA molecules specifically induced by the hormone in the nucleus have been identified. Nuclear RNA from intestine of vitamin D-deficient chicks before and at various time intervals after treatment with the hormone or cholecalciferol was tested for its ability to code for calcium-binding protein in a cell-free system. Calcium-binding-protein mRNA could only just be detected in the intestinal nuclei 2h after dosing with these steroids which is the same time that it was first observed in the polyribosomes. Thus 1,25-dihydroxycholecalciferol induces the production of new calcium-binding protein by stimulating the formation and rapid release from the nucleus of new mRNA molecules for this protein. Polyribosomal translation of the mRNA continued only as long as it was being synthesized, and the maximum rate of synthesis following a pulse dose of 125ng of the hormone was the same as that observed after prolonged stimulation with cholecalciferol. The possibility that other 1,25-dihydroxycholecalciferol-dependent events may be occurring in the nucleus in the lag period between accumulation of the hormone in the intestine and the appearance of active calcium-binding-protein mRNA, and that these may ultimately control the synthesis of that mRNA, is discussed.

Influence of vitamin D on calcium absorption in the chick

1962 ◽  
Vol 203 (3) ◽  
pp. 497-505 ◽  
Author(s):  
J. D. Sallis ◽  
E. S. Holdsworth
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Metabolic Inhibitors ◽  
Hydroxyl Groups ◽  
Oxidation Reduction ◽  
Active Calcium

The site of absorption of Ca45 was studied in rachitic chicks and rachitic chicks given vitamin D3. Vitamin D3 markedly increases absorption from the small intestine and, in vivo, similar amounts of calcium are absorbed along the entire small intestine. With everted gut sacs, the distal third of the small intestine transported much more calcium than did the duodenal and middle sections. Thus, interpretations of in vitro results may not always depict the natural in vivo process. Vitamin D2 had little activity in the chick, but AT-10 series 2 and AT-10 series 3 were almost as active as vitamin D3 for calcium transport. These results suggest an "active carrier" may be formed by addition of hydrogen or hydroxyl groups to the opened ring B of vitamin D, giving a carrier capable of reversible oxidation-reduction or keto-enol tautomerism. Using metabolic inhibitors, active calcium transport in vitro relied on glycolysis for its energy supply. The transport was independent of the sodium pump.

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