Endurance swimming stimulates transepithelial calcium transport and alters the expression of genes related to calcium absorption in the intestine of rats

2009 ◽  
Vol 296 (4) ◽  
pp. E775-E786 ◽  
Author(s):  
Jarinthorn Teerapornpuntakit ◽  
Nitita Dorkkam ◽  
Kannikar Wongdee ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Relevant Information ◽  
Proximal Colon ◽  
Intestinal Calcium Absorption ◽  
Proximal Jejunum ◽  
Microarray Study ◽  
Expression Of Genes ◽  
Impact Exercise ◽  
Calbindin D

Endurance impact exercise, e.g., running, is known to enhance the intestinal calcium absorption. However, nonimpact exercise, e.g., swimming, is more appropriate for osteoporotic patients with cardiovascular diseases or disorders of bone and joint, but the effect of swimming on the intestinal calcium transport was unknown. This study, therefore, aimed to investigate the transepithelial calcium transport and the expression of related genes in the intestine of rats trained to swim nonstop 1 h/day, 5 days/wk for 2 wk. We found that endurance swimming stimulated calcium transport in the duodenum, proximal jejunum, and cecum, while decreasing that in the proximal colon. Swimming affected neither the transepithelial potential difference nor resistance. As demonstrated by real-time PCR, the small intestine, especially the duodenum, responded to swimming by upregulating a number of genes related to the transcellular calcium transport, i.e., TRPV5, TRPV6, calbindin-D9k, PMCA1b, and NCX1, and the paracellular calcium transport, i.e., ZO-1, ZO-2, ZO-3, cingulin, occludin, and claudins, as well as nuclear receptor of 1,25(OH)2D3. In contrast, swimming downregulated those genes in the colon. Microarray analysis showed that swimming also altered the expression of duodenal genes related to the transport of several ions and nutrients, e.g., Na+, K+, Cl−, glucose, and amino acids. In conclusion, endurance swimming enhanced intestinal calcium absorption, in part, by upregulating the calcium transporter genes. The present microarray study also provided relevant information for further investigations into the intestinal nutrient and electrolyte transport during nonimpact exercise.

Comparison of calcium absorptive and secretory capacities of segments of intact or functionally resected intestine during normo-, hypo-, and hyper-calcemia

1994 ◽  
Vol 72 (7) ◽  
pp. 764-770 ◽  
Author(s):  
N. Krishnamra ◽  
K. Angkanaporn ◽  
T. Deenoi
Keyword(s):  
Calcium Absorption ◽  
Intestinal Secretion ◽  
Proximal Colon ◽  
Plasma Calcium ◽  
Proximal Jejunum ◽  
Proximal Small Intestine ◽  
Enhanced Secretion ◽  
Rate Of Absorption ◽  
Plasma Calcium Concentration ◽  
Luminal Calcium

Absorptive and secretory capacities of six in situ intestinal loops of equal length were compared under the same calcium load and calcemic condition. The highest rate of calcium absorption was found in duodenum, colon, and proximal jejunum when loops were filled with 0.3 mM calcium, and in duodenum and proximal jejunum when filled with 10 mM luminal calcium. Secretory rates were in the following order: duodenum, jejunum, proximal jejunum, cecum, ileum, and proximal colon. Absorption of 0.3 mM calcium was decreased in all but the cecum and colon during hypercalcemia, and in duodenum, proximal jejunum, and colon during thyroparathyroidectomy-induced hypocalcemia. In contrast, calcium secretion was directly related to plasma calcium concentration and the length of the intestine. Functional resection of any part met with a compensatory increase in calcium absorption by the remaining segments, with the exception of the resection of the distal ileum with the large bowel. In conclusion, proximal small intestine exhibited the highest rate of absorption and secretion, but functional resection of this or any part did not affect the overall calcium absorption if luminal calcium was 10 mM. Moreover, enhanced secretion and reduced absorption during hypercalcemia were beneficial with respect to plasma calcium regulation.Key words: calcium, hypercalcemia, hypocalcemia, intestinal absorption, intestinal secretion.

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.

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

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.

Impaired body calcium metabolism with low bone density and compensatory colonic calcium absorption in cecectomized rats

2012 ◽  
Vol 302 (7) ◽  
pp. E852-E863 ◽  
Author(s):  
Prapaporn Jongwattanapisan ◽  
Panan Suntornsaratoon ◽  
Kannikar Wongdee ◽  
Nitita Dorkkam ◽  
Nateetip Krishnamra ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Calcium Transport ◽  
Calcium Metabolism ◽  
Calcium Absorption ◽  
Calcium Excretion ◽  
Compensatory Mechanism ◽  
Calcium Balance ◽  
Balance Study ◽  
Colonic Epithelial Cells ◽  
Calbindin D

An earlier study reported that cecal calcium absorption contributes less than 10% of total calcium absorbed by the intestine, although the cecum has the highest calcium transport rate compared with other intestinal segments. Thus, the physiological significance of the cecum pertaining to body calcium metabolism remains elusive. Herein, a 4-wk calcium balance study in cecectomized rats revealed an increase in fecal calcium loss with marked decreases in fractional calcium absorption and urinary calcium excretion only in the early days post-operation, suggesting the presence of a compensatory mechanism to minimize intestinal calcium wasting. Further investigation in cecectomized rats showed that active calcium transport was enhanced in the proximal colon but not in the small intestine, whereas passive calcium transport along the whole intestine was unaltered. Since apical exposure to calcium-sensing receptor (CaSR) agonists similarly increased proximal colonic calcium transport, activation of apical CaSR in colonic epithelial cells could have been involved in this hyperabsorption. Calcium transporter genes, i.e., TRPV6 and calbindin-D9k, were also upregulated in proximal colonic epithelial cells. Surprisingly, elevated serum parathyroid hormone levels and hyperphosphatemia were evident in cecectomized rats despite normal plasma calcium levels, suggesting that colonic compensation alone might be insufficient to maintain normocalcemia. Thus, massive bone loss occurred in both cortical and trabecular sites, including lumbar vertebrae, femora, and tibiae. The presence of compensatory colonic calcium hyperabsorption with pervasive osteopenia in cecectomized rats therefore corroborates that the cecum is extremely crucial for body calcium homeostasis.

Fibroblast growth factor-23 abolishes 1,25-dihydroxyvitamin D3-enhanced duodenal calcium transport in male mice

2012 ◽  
Vol 302 (8) ◽  
pp. E903-E913 ◽  
Author(s):  
Pissared Khuituan ◽  
Jarinthorn Teerapornpuntakit ◽  
Kannikar Wongdee ◽  
Panan Suntornsaratoon ◽  
Nipaporn Konthapakdee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Fibroblast Growth Factor ◽  
Calcium Absorption ◽  
Ussing Chamber ◽  
Intestinal Calcium Absorption ◽  
Fibroblast Growth ◽  
Male Mice ◽  
Calbindin D ◽  
Fgf 23

Despite being widely recognized as the important bone-derived phosphaturic hormone, whether fibroblast growth factor (FGF)-23 modulated intestinal calcium absorption remained elusive. Since FGF-23 could reduce the circulating level of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], FGF-23 probably compromised the 1,25(OH)2D3-induced intestinal calcium absorption. FGF-23 may also exert an inhibitory action directly through FGF receptors (FGFR) in the intestinal cells. Herein, we demonstrated by Ussing chamber technique that male mice administered 1 μg/kg 1,25(OH)2D3 sc daily for 3 days exhibited increased duodenal calcium absorption, which was abolished by concurrent intravenous injection of recombinant mouse FGF-23. This FGF-23 administration had no effect on the background epithelial electrical properties, i.e., short-circuit current, transepithelial potential difference, and resistance. Immunohistochemical evidence of protein expressions of FGFR isoforms 1–4 in mouse duodenal epithelial cells suggested a possible direct effect of FGF-23 on the intestine. This was supported by the findings that FGF-23 directly added to the serosal compartment of the Ussing chamber and completely abolished the 1,25(OH)2D3-induced calcium absorption in the duodenal tissues taken from the 1,25(OH)2D3-treated mice. However, direct FGF-23 exposure did not decrease the duodenal calcium absorption without 1,25(OH)2D3 preinjection. The observed FGF-23 action was mediated by MAPK/ERK, p38 MAPK, and PKC. Quantitative real-time PCR further showed that FGF-23 diminished the 1,25(OH)2D3-induced upregulation of TRPV5, TRPV6, and calbindin-D9k, but not PMCA1b expression in the duodenal epithelial cells. In conclusion, besides being a phosphatonin, FGF-23 was shown to be a novel calcium-regulating hormone that acted directly on the mouse intestine, thereby compromising the 1,25(OH)2D3-induced calcium absorption.

Enhancement of calcium transport in Caco-2 monolayer through PKCζ-dependent Cav1.3-mediated transcellular and rectifying paracellular pathways by prolactin

2009 ◽  
Vol 296 (6) ◽  
pp. C1373-C1382 ◽  
Author(s):  
Narongrit Thongon ◽  
La-iad Nakkrasae ◽  
Jirawan Thongbunchoo ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Protein Biosynthesis ◽  
Ussing Chamber ◽  
Calcium Flux ◽  
Channel Blockers ◽  
Voltage Dependent ◽  
Calbindin D

Previous investigations suggested that prolactin (PRL) stimulated the intestinal calcium absorption through phosphoinositide 3-kinase (PI3K), protein kinase C (PKC), and RhoA-associated coiled-coil forming kinase (ROCK) signaling pathways. However, little was known regarding its detailed mechanisms for the stimulation of transcellular and voltage-dependent paracellular calcium transport. By using Ussing chamber technique, we found that the PRL-induced increase in the transcellular calcium flux and decrease in transepithelial resistance of intestinal-like Caco-2 monolayer were not abolished by inhibitors of gene transcription and protein biosynthesis. The PRL-stimulated transcellular calcium transport was completely inhibited by the L-type calcium channel blockers (nifedipine and verapamil) and plasma membrane Ca2+-ATPase (PMCA) inhibitor (trifluoperazine) as well as small interfering RNA targeting voltage-dependent L-type calcium channel Cav1.3, but not TRPV6 or calbindin-D9k. As demonstrated by 45Ca uptake study, PI3K and PKC, but not ROCK, were essential for the PRL-enhanced apical calcium entry. In addition, PRL was unable to enhance the transcellular calcium transport after PKCζ knockdown or exposure to inhibitors of PKCζ, but not of PKCα, PKCβ, PKCε, PKCμ, or protein kinase A. Voltage-clamping experiments further showed that PRL markedly stimulated the voltage-dependent calcium transport and removed the paracellular rectification. Such PRL effects on paracellular transport were completely abolished by inhibitors of PI3K (LY-294002) and ROCK (Y-27632). It could be concluded that the PRL-stimulated transcellular calcium transport in Caco-2 monolayer was mediated by Cav1.3 and PMCA, presumably through PI3K and PKCζ pathways, while the enhanced voltage-dependent calcium transport occurred through PI3K and ROCK pathways.

Prolactin is an important regulator of intestinal calcium transport

2007 ◽  
Vol 85 (6) ◽  
pp. 569-581 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Nateetip Krishnamra
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption ◽  
The Body ◽  
Female Rats ◽  
Calcium Excretion ◽  
Target Tissue ◽  
Intestinal Calcium Transport

Prolactin has been shown to stimulate intestinal calcium absorption, increase bone turnover, and reduce renal calcium excretion. The small intestine, which is the sole organ supplying new calcium to the body, intensely expresses mRNAs and proteins of prolactin receptors, especially in the duodenum and jejunum, indicating the intestine as a target tissue of prolactin. A number of investigations show that prolactin is able to stimulate the intestinal calcium transport both in vitro and in vivo, whereas bromocriptine, which inhibits pituitary prolactin secretion, antagonizes its actions. In female rats, acute and long-term exposure to high prolactin levels significantly enhances the (i) transcellular active, (ii) solvent drag-induced, and (iii) passive calcium transport occurring in the small intestine. These effects are seen not only in pregnant and lactating animals, but are also observed in non-pregnant and non-lactating animals. Interestingly, young animals are more responsive to prolactin than adults. Prolactin-enhanced calcium absorption gradually diminishes with age, thus suggesting it has an age-dependent mode of action. Although prolactin's effects on calcium absorption are not directly vitamin D-dependent; a certain level of circulating vitamin D may be required for the basal expression of genes related to calcium transport. The aforementioned body of evidence supports the hypothesis that prolactin acts as a regulator of calcium homeostasis by controlling the intestinal calcium absorption. Cellular and molecular signal transductions of prolactin in the enterocytes are largely unknown, however, and still require investigation.

scholarly journals Impaired renal calcium absorption in mice lacking calcium channel β3 subunits

2009 ◽  
Vol 87 (7) ◽  
pp. 522-530 ◽  
Author(s):  
José F. Bernardo ◽  
Clara E. Magyar ◽  
W. Bruce Sneddon ◽  
Peter A. Friedman
Keyword(s):  
Plasma Membrane ◽  
Transgenic Mice ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Sodium Excretion ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Wild Type ◽  
Distal Tubules ◽  
Calbindin D

Transgenic mice lacking calcium channel β3 subunits (CaVβ3) were used to determine the involvement of a multimeric calcium channel in mediating stimulated renal calcium absorption. We measured the ability of calcium channel β3 subunit-null (CaVβ3−/−) and wild-type (CaVβ3+/+) mice to increase renal calcium absorption in response to the calcium-sparing diuretic chlorothiazide (CTZ). Control rates of fractional sodium excretion were comparable in CaVβ3−/− and CaVβ3+/+ mice and CTZ increased sodium excretion similarly in both groups. CTZ enhanced calcium absorption only in wild-type CaVβ3+/+ mice. This effect was specific for diuretics acting on distal tubules because both CaVβ3−/− and CaVβ3+/+ mice responded comparably to furosemide. The absence of β3 subunits resulted in compensatory increases of TrpV5 calcium channels, the plasma membrane Ca-ATPase, NCX1 Na/Ca exchanger protein, and calbindin-D9k but not calbindin-D28k. We conclude that TrpV5 mediates basal renal calcium absorption and that a multimeric calcium channel that includes CaVβ3 mediates stimulated calcium transport.

Sign in / Sign up

Export Citation Format

Share Document