scholarly journals Prolactin directly stimulated the solvent drag-induced calcium transport in the duodenum of female rats

2004 ◽  
Vol 1665 (1-2) ◽  
pp. 81-91 ◽  
Author(s):  
Chaiyot Tanrattana ◽  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Calcium Transport ◽  
Female Rats ◽  
Solvent Drag

scholarly journals 1,25-Dihydroxyvitamin D3 Rapidly Stimulates the Solvent Drag–Induced Paracellular Calcium Transport in the Duodenum of Female Rats

2008 ◽  
Vol 58 (5) ◽  
pp. 297-307 ◽  
Author(s):  
Kukiat Tudpor ◽  
Jarinthorn Teerapornpuntakit ◽  
Walailuk Jantarajit ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Calcium Transport ◽  
Female Rats ◽  
Solvent Drag ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3

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.

Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats

2001 ◽  
Vol 79 (5) ◽  
pp. 430-438 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Direct Action ◽  
Female Rats ◽  
Calcium Flux ◽  
Total Calcium ◽  
Solvent Drag ◽  
Control Value ◽  
Voltage Dependent ◽  
Active Calcium

Prolactin has been postulated to be a novel calcium-regulating hormone during pregnancy and lactation. It stimulates both passive and active duodenal calcium transport in several experimental models. Our study was performed on sexually mature female Wistar rats (200–250 g) to study the direct action of prolactin on calcium transport in the duodenum using the Ussing chamber technique. To evaluate the effect of prolactin on total calcium transport in the duodenum, we intraperitoneally injected rats with 0.4, 0.6, and 0.8 mg/kg prolactin. The total calcium transport was divided into voltage-dependent, solvent drag-induced, and transcellular active fluxes by applying short-circuit current and by mucosal glucose replacement with mannitol. The effect of prolactin on each flux was studied separately. Finally, to evaluate the direct action of prolactin on duodenal transcellular active flux, we directly exposed duodenal segments to prolactin that had been added to the serosal solution with or without calcium transport inhibitors. We found that 0.6 and 0.8 mg/kg prolactin ip significantly increased the total mucosa–to–serosa calcium flux from the control value (nmol·hr–1·cm–2) of 34.53 ± 6.81 to 68.07 ± 13.53 (P < 0.05) and 84.43 ± 19.72 (P < 0.01), respectively. Prolactin also enhanced the solvent drag-induced calcium flux and transcellular active calcium flux, but not the voltage-dependent calcium flux. The duodenal segments directly exposed to 200, 400, and 800 ng/mL prolactin showed a significant increase in the transcellular active calcium absorption in a dose-dependent manner, i.e., from the control value (nmol·hr–1·cm–2) of 2.94 ± 0.47 to 5.45 ± 0.97 (P < 0.01), 8.09 ± 0.52 (P < 0.001), and 18.42 ± 2.92 (P < 0.001), respectively. Its direct action was inhibited by mucosal exposure to 50 µM lanthanum chloride, a calcium transporter protein competitor, and serosal exposure to 0.1 mM trifluoperazine, a Ca2+-ATPase inhibitor. These studies demonstrate that the duodenum is a target organ of prolactin, which enhances transcellular active calcium transport.Key words: calcium absorption, duodenum, prolactin, solvent drag, transcellular calcium transport.

Long-Term Prolactin Exposure Differentially Stimulated the Transcellular and Solvent Drag-Induced Calcium Transport in the Duodenum of Ovariectomized Rats

2005 ◽  
Vol 230 (11) ◽  
pp. 836-844 ◽  
Author(s):  
Kukiat Tudpor ◽  
Narattaphol Charoenphandhu ◽  
Wasana Saengamnart ◽  
Nateetip Krishnamra
Keyword(s):  
Calcium Transport ◽  
Ovariectomized Rats ◽  
Solvent Drag

Prolactin directly enhanced Na+/K+- and Ca2+-ATPase activities in the duodenum of female rats

2006 ◽  
Vol 84 (5) ◽  
pp. 555-563 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Atpase Activity ◽  
Brush Border ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Basolateral Membrane ◽  
Female Rats ◽  
Dependent Manner ◽  
Control Value ◽  
Crude Homogenate ◽  
Active Calcium

Prolactin has recently been shown to directly stimulate 2 components of the active duodenal calcium transport in female rats, i.e., solvent drag-induced and transcellular-active calcium transport. Since the basolateral Na+/K+- and Ca2+-ATPases, respectively, play important roles in these 2 transport mechanisms, the present study aimed to examine the direct actions of prolactin on the activities of both transporters in sexually mature female Wistar rats. The results showed that 200, 400, and 800 ng/mL prolactin produced a significant increase in the total ATPase activity of duodenal crude homogenate in a dose-dependent manner within 60 min (i.e., from a control value of 1.53 ± 0.13 to 2.29 ± 0.21 (p < 0.05), 2.68 ± 0.19 (p < 0.01), and 3.92 ± 0.33 (p < 0.001) µmol Pi·(mg protein)–1·min–1, respectively). Activity of Na+/K+-ATPase was increased by 800 ng/mL prolactin from 0.17 ± 0.03 to 1.18 ± 0.29 µmol Pi·(mg protein)–1·min–1 (p < 0.01). Prolactin at doses of 400 and 600 ng/mL also significantly increased the activities of Ca2+-ATPase in crude homogenate from a control value of 0.84 ± 0.03 to 1.75 ± 0.29 (p < 0.05), and 2.30 ± 0.37 (p < 0.001) µmol Pi·(mg protein)–1·min–1. When the crude homogenate was purified for the basolateral membrane, the Na+/K+-ATPase activities were elevated 10-fold. In the purified homogenate, 800 ng/mL prolactin increased Na+/K+-ATPase activity from 1.79 ± 0.38 to 2.63 ± 0.44 µmol Pi·(mg protein)–1·min–1 (p < 0.05), and Ca2+-ATPase activity from 0.08 ± 0.14 to 2.03 ± 0.23 µmol Pi·(mg protein)–1·min–1 (p < 0.001). Because the apical calcium entry was the first important step for the transcellular active calcium transport, the brush border calcium uptake was also investigated in this study. We found that, 8 min after being directly exposed to 800 ng/mL prolactin, the brush border calcium uptake into the duodenal epithelial cells was increased from 0.31 ± 0.02 to 0.80 ± 0.28 nmol·(mg protein)–1 (p < 0.05). It was concluded that prolactin directly and rapidly enhanced the brush border calcium uptake as well as the activities of the basolateral Na+/K+- and Ca2+-ATPases in the duodenal epithelium of female rats. These findings explained the mechanisms by which prolactin stimulated duodenal active calcium absorption.

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.

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