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

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.

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.


1977 ◽  
Vol 232 (2) ◽  
pp. E229
Author(s):  
E L Krawitt ◽  
A S Kunin ◽  
H W Sampson ◽  
B F Bacon

To examine the effect of hypophysectomy on intestinal calcium absorption, studies were performed on immature rats 7, 14, and 21 days after hypophysectomy. Duodenal calcium transport was measured in vitro utilizing everted gut sacs and in vivo by a luminal perfusion technique. Hypophysectomy produced no differences in the ability of everted gut sacs to transport calcium. Similarly, when in vivo transport data were expressed on the basis of intestinal length, no significant differences were noted. However, when transport data were expressed on the basis of mucosal weight, increases in absorption and lumen-to-plasma fluxes were apparent in hypophysectomized animals. No differences were seen in plasma-to-lumen fluxes. The results indicate that when the transport data are corrected for mass of intestinal mucosa, the duodenum from hypophysectomized animals absorbs calcium more avidly due to an increase in lumen-to-plasma flux.


1984 ◽  
Vol 246 (3) ◽  
pp. G268-G273
Author(s):  
M. J. Favus ◽  
C. B. Langman

To determine whether prior vitamin D intake influences the intestinal calcium absorptive action of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], we measured in vitro the two unidirectional transepithelial fluxes of calcium across descending colon segments from rats fed either a vitamin D-deficient or normal diet and injected with either 10, 25, or 75 ng of 1,25(OH)2D3 or vehicle alone. Vitamin D deficiency abolished net calcium absorption [J net, -2 +/- 2 vs. 12 +/- 2 (SE) nmol X cm-2 X h-1, P less than 0.001], and 10 ng of 1,25(OH)2D3 raised J net to levels found in normal rats. Larger doses (25 and 75 ng) increased J net above levels in normal rats given the same dose. In normal rats only 75 ng of 1,25(OH)2D3 increased calcium J net above vehicle control values (12 +/- 2 vs. 38 +/- 4 nmol X cm-2 X h-1, P less than 0.001). Circulating 1,25(OH)2D3 measured by radioreceptor assay was well correlated with calcium transport. For each dose of 1,25(OH)2D3 higher serum 1,25(OH)2D3 levels were reached in vitamin D-deficient rats. Only the 75-ng dose increased circulating 1,25(OH)2D3 and colonic calcium transport in normal rats. Intravenous [3H]-1,25(OH)2D3 disappeared more rapidly from the circulation of normal rats, suggesting that accelerated metabolic degradative processes for 1,25(OH)2D3 may be present in normal but not in vitamin D-deficient rats and may account for the lack of a biological response to 1,25(OH)2D3 in normal animals.


1985 ◽  
Vol 248 (6) ◽  
pp. G676-G681 ◽  
Author(s):  
M. J. Favus ◽  
E. Angeid-Backman

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.


1988 ◽  
Vol 255 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
K. M. Carroll ◽  
R. J. Wood ◽  
E. B. Chang ◽  
I. H. Rosenberg

Glucose stimulates calcium transport in vitro in rat duodenal tissue and isolated enterocytes. Under short-circuited conditions, glucose increased mucosal to serosal calcium flux (JCa(m----s)) without altering serosal to mucosal calcium flux (JCa(s----m)) in the duodenum, the primary site of active calcium absorption in the rat small intestine. The half-maximal dose (ED50) of the glucose stimulatory effect was less than 1 mM, and an increase in JCa(m----s) of 80% over control was seen at a glucose concentration of 50 mM. Glucose did not increase calcium flux in the ileum where active calcium absorption is minimal. Glucose stimulated net calcium uptake by 35% in isolated duodenal enterocytes. Glucose did not alter calcium efflux from preloaded enterocytes suspended in calcium-free buffer. Glucose enhancement of net calcium uptake in enterocytes was not caused by altered cell membrane integrity or functional viability. The nonmetabolizable glucose analogue alpha-methylglucoside did not stimulate calcium transport. Our findings suggest that glucose can stimulate intestinal calcium absorption, at least partially, by enhancing transcellular calcium transport and that cellular glucose metabolism is necessary for stimulation of this route of calcium transport.


2002 ◽  
Vol 42 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Takaharu Kozakai ◽  
Norio Uozumi ◽  
Kazuo Katoh ◽  
Yoshiaki Obara

1958 ◽  
Vol 194 (2) ◽  
pp. 319-326 ◽  
Author(s):  
Elmer B. Brown ◽  
Bertram W. Justus

Everted pouches of rat intestine prepared by the technique of Wilson and associates were used to measure absorption of radioiron. Iron was taken up equally well in vitro by all segments of the rat's small intestine; but when the iron was given orally in vivo, a distinct gradient, highest in the duodenum and progressively smaller in the distal segments was demonstrated. There was little transfer into the inner serosal pouch. Transfer of iron in this preparation was by a process of passive transport. It was not appreciably affected by changes in pH, various metabolic inhibitors, buffer systems, or added substrates. Ferrous iron was significantly better taken up by the intestinal tissue, but transfer into the inner pouch fluid was greater with ferric iron.


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