Stimulation of intestinal calcium transport and bone calcium mobilization by prolactin in vitamin D-deficient rats

Science ◽  
1981 ◽  
Vol 214 (4524) ◽  
pp. 1038-1039 ◽  
Author(s):  
D. Pahuja ◽  
H. DeLuca
Keyword(s):  
Vitamin D ◽  
Calcium Transport ◽  
Calcium Mobilization ◽  
Intestinal Calcium Transport ◽  
Bone Calcium ◽  
Stimulation Of

1-Fluorovitamin D3, a vitamin D3 analog more active on bone-calcium mobilization than on intestinal-calcium transport

Biochemistry ◽  
1979 ◽  
Vol 18 (9) ◽  
pp. 1641-1646 ◽  
Author(s):  
Joseph L. Napoli ◽  
Mary A. Fivizzani ◽  
Heinrich K. Schnoes ◽  
Hector F. DeLuca
Keyword(s):  
Vitamin D3 ◽  
Calcium Transport ◽  
Calcium Mobilization ◽  
Intestinal Calcium Transport ◽  
Bone Calcium

Bone changes due to pregnancy and lactation: influence of vitamin D status

1986 ◽  
Vol 251 (4) ◽  
pp. E400-E406 ◽  
Author(s):  
P. J. Marie ◽  
L. Cancela ◽  
N. Le Boulch ◽  
L. Miravet
Keyword(s):  
Vitamin D ◽  
Bone Resorption ◽  
Bone Formation ◽  
Trabecular Bone ◽  
Formation Rate ◽  
Vitamin D Status ◽  
Bone Formation Rate ◽  
Bone Calcium ◽  
Pregnancy And Lactation ◽  
Stimulation Of

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.

Mechanism of regulation of calcium-pumping activity in chick intestine

1992 ◽  
Vol 262 (5) ◽  
pp. G797-G805
Author(s):  
J. Takito ◽  
T. Shinki ◽  
H. Tanaka ◽  
T. Suda
Keyword(s):  
Vitamin D ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Early Stage ◽  
Basolateral Membrane ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Membrane Vesicles ◽  
Intestinal Calcium Transport ◽  
Pumping Activity

The role of the calcium pump in the stimulation of intestinal calcium transport activity by 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] was examined in chicks. The in situ intestinal absorption of calcium increased approximately threefold in the duodenum, jejunum, and ileum 6 h after a single injection of 625 ng of 1 alpha,25(OH)2D3 into vitamin D-deficient chicks. The same treatment also increased approximately twofold the rate of ATP-dependent calcium uptake by the basolateral membrane vesicles (BL) isolated from those three sites. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that a Mg(2+)-dependent calcium-stimulated phosphorylated intermediate with an apparent molecular mass of 105 kDa appeared in the BL. The 1 alpha,25(OH)2D3 treatment gave no change in the levels of the intermediate. Pretreatment of the BL with alkaline phosphatase decreased the calcium uptake by the BL isolated from 1 alpha,25(OH)2D3-treated chicks, but it had little effect on the uptake by the BL from vitamin D-deficient chicks. These results suggest that at an early stage of the 1 alpha,25(OH)2D3-induced intestinal calcium transport process, the vitamin regulates the calcium-pumping activity of chick intestinal BL by phosphorylation and dephosphorylation but not by a stoichiometric change in the pump.

Biological activity of 1,25-dihydroxyvitamin D2 and 24-epi-1,25-dihydroxyvitamin D2

1988 ◽  
Vol 254 (4) ◽  
pp. E402-E406
Author(s):  
H. F. DeLuca ◽  
R. R. Sicinski ◽  
Y. Tanaka ◽  
P. H. Stern ◽  
C. M. Smith
Keyword(s):  
Biological Activity ◽  
Calcium Transport ◽  
Inorganic Phosphorus ◽  
Short Term ◽  
Dihydroxyvitamin D3 ◽  
Intestinal Calcium Transport ◽  
Fetal Rat ◽  
Bone Calcium ◽  
Biological Effectiveness

The biological activity of 1,25-dihydroxyvitamin D2 [1,25(OH)2D2] and 24-epi-1,25-dihydroxyvitamin D2 [24-epi-1,25(OH)2D2] has been determined in vitamin D-deficient rats. The biological effectiveness of 1,25(OH)2D2 is equal to that reported previously for 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] (15) in intestinal calcium transport, mineralization of bone, mobilization of bone calcium, and elevation of plasma inorganic phosphorus of rachitic rats. However, 24-epi-1,25(OH)2D2 is at best one-half as active as 1,25(OH)2D2 in stimulating intestinal calcium transport and in the mineralization of rachitic bone. The 24-epi-1,25(OH)2D2 is one-third as active as 1,25(OH)2D3 in binding to the chick intestinal receptor for 1,25(OH)2D3. Thus receptor discrimination may account for the twofold difference in intestinal calcium transport activity. 24-Epi-1,25(OH)2D2 appeared inactive in in vivo mobilization of bone calcium or bone phosphorus. On the other hand, in fetal rat bone in culture, the epi compound was only five times less active than 1,25(OH)2D2 in inducing resorption. Short-term experiments on bone mineral mobilization in vivo show that the 24-epi-1,25(OH)2D2 does induce bone calcium mobilization but that its activity in this respect is short lived. It is suggested that 24-epi-1,25(OH)2D2 and, as a result, it shows preferential activity on intestine whose response to a single dose of 1,25(OH)2D2 remains for several days, whereas the short-lived bone system does not remain stimulated during the 24-h period between doses.

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