Direct stimulating action of blood serum and of vitamin D3 and its hydroxy-analogs on calcium transport in the chicken small intestine in vitro

1980 ◽  
Vol 90 (6) ◽  
pp. 1676-1679 ◽  
Author(s):  
V. K. Bauman ◽  
R. E. Andrushaite ◽  
N. I. Berzin' ◽  
M. Yu. Valinietse ◽  
A. R. Val'dman
1986 ◽  
Vol 250 (4) ◽  
pp. G412-G419
Author(s):  
H. P. Schedl ◽  
D. L. Miller ◽  
R. L. Horst ◽  
H. D. Wilson ◽  
K. Natarajan ◽  
...  

We previously found intestinal Ca2+ transport to be lower in the spontaneously hypertensive (SH) as compared with the Wistar-Kyoto control (WKY) rat. These animals were fed a relatively high (1%) Ca2+ diet, and the concentration of 1 alpha,25-dihydroxycholecalciferol [1 alpha,25(OH)2D3] in serum was the same in both groups. In the present experiment we tested the possibility that the lower Ca2+ transport in the SH rat was the result of unresponsiveness to 1 alpha,25(OH)2D3. We fed diets high and low in Ca2+ and measured serum 1 alpha,25(OH)2D3 and Ca2+ transport. Serum 1 alpha,25(OH)2D3 increased in response to Ca2+ depletion at both 5 and 12 wk in both the WKY and SH rat. With high-Ca2+ diet, Ca2+ transport was lower in SH than in WKY when studied 1) in vitro in duodenum at 5 wk of age, and 2) in vivo in proximal and distal small intestine at 12 wk of age. Ca2+ transport increased in SH in response to Ca2+ depletion, but not in WKY, except in distal small intestine in vivo at 12 wk. In summary, although Ca2+ transport is lower in the SH as compared with the WKY rat when vitamin D activity is basal through feeding a high-Ca2+ diet, Ca2+ transport increases in the SH rat in response to the increase in 1 alpha,25(OH)2D3 produced by feeding a low-Ca2+ diet. We conclude that 1) the vitamin D-regulated component of mediated Ca2+ transport is intact in the SH rat and is unrelated to hypertension, and 2) mediated Ca2+ transport under basal conditions, i.e., nonvitamin D-regulated, differs in the SH and WKY rats and may be related to hypertension.


1975 ◽  
Vol 64 (1) ◽  
pp. 54-74 ◽  
Author(s):  
R R Warner ◽  
J R Coleman

Calcium transport in small intestine of rat and chick has been studied at the cellular level using the electron probe X-ray microanalyzer. Tissues were examined directly after removal as well as after incubation in a calcium solution. In both preparations, discrete calcium localizations were found associated with intracellular and extracellular goblet cell mucus. The in vitro preparations showed calcium in transit across the absorptive epithelium in discrete localizations. Although the primary path of transport was along lateral cell borders, some localizations were found in the cytoplasm in a supranuclear position. The effect of vitamin D depletion and repletion was to decrease and increase, respectively, the number of calcium localizations in transit across the epithelium. These results suggest that calcium is transported while in a sequestered form and indicate that goblet cell mucus plays a role in this transport process.


1960 ◽  
Vol 199 (2) ◽  
pp. 265-271 ◽  
Author(s):  
Harold E. Harrison ◽  
Helen C. Harrison

The transfer of calcium across the intestinal wall of rats was measured in vitro by the device of everted intestinal loops with Ca45 as an indicator. The conditions were developed so that the rate of diffusion of calcium across the intestinal wall as well as active transport against a concentration gradient could be determined. Vitamin D treatment increases the rate of diffusion of calcium across the intestinal wall. This action of vitamin D is exerted along the entire length of the small intestine and is not affected by inhibition of oxidative metabolism. The active transport of calcium on the other hand is localized to the proximal part of the intestine and is dependent on the energy of oxidative metabolism. Cortisol treatment antagonizes the vitamin D effect on the diffusion of calcium and also reduces the active transport of calcium. It is suggested that vitamin D and cortisol influence calcium transport by action on the permeability of cell surfaces to calcium.


1962 ◽  
Vol 203 (3) ◽  
pp. 497-505 ◽  
Author(s):  
J. D. Sallis ◽  
E. S. Holdsworth

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.


Author(s):  
A. J. Tousimis

The elemental composition of amino acids is similar to that of the major structural components of the epithelial cells of the small intestine and other tissues. Therefore, their subcellular localization and concentration measurements are not possible by x-ray microanalysis. Radioactive isotope labeling: I131-tyrosine, Se75-methionine and S35-methionine have been successfully employed in numerous absorption and transport studies. The latter two have been utilized both in vitro and vivo, with similar results in the hamster and human small intestine. Non-radioactive Selenomethionine, since its absorption/transport behavior is assumed to be the same as that of Se75- methionine and S75-methionine could serve as a compound tracer for this amino acid.


1987 ◽  
Vol 5 (2) ◽  
pp. 292-298 ◽  
Author(s):  
R P Warrell ◽  
N W Alcock ◽  
R S Bockman

Bone metastases are a major source of morbidity in patients with cancer. Previously, we found that gallium nitrate was a highly effective treatment for cancer-related hypercalcemia. Laboratory studies have shown that this drug inhibits bone resorption in vitro and that short-term treatment in vivo increases the calcium content of bone. We evaluated the clinical effects of gallium nitrate on biochemical parameters of increased bone turnover in 22 patients with bone metastases. Treatment with gallium nitrate for five to seven days caused a median reduction in 24-hour urinary calcium excretion of 66% relative to baseline measurements (P less than .01). Hydroxyproline (OHP) excretion was also significantly reduced (P less than .01). The greatest reduction in hydroxyprolinuria occurred in patients with high baseline excretion. Ionized serum calcium and serum phosphorous declined significantly after treatment (P less than .01 for each). Serum immunoreactive parathyroid hormone (PTH) increased significantly (P less than .01), as did serum levels of 1,25 (OH)2-vitamin D3 (P less than .05). Urinary phosphorous excretion and serum levels of 25-OH-vitamin D3 were not significantly changed. No major toxic reactions occurred as a result of this treatment. These results indicate that gallium nitrate significantly reduces biochemical parameters associated with accelerated bone turnover and that this agent may be useful for preventing pathologic conditions associated with bone metastases.


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