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

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.

25,26-Dihydroxycholecalciferol, a metabolite of vitamin D3 with intestinal calcium transport activity

Biochemistry ◽  
1970 ◽  
Vol 9 (24) ◽  
pp. 4776-4780 ◽  
Author(s):  
Hector F. DeLuca ◽  
Tatsuo Suda ◽  
Heinrich K. Schnoes ◽  
Yoko Tanaka ◽  
Michael F. Holick
Keyword(s):  
Vitamin D3 ◽  
Calcium Transport ◽  
Transport Activity ◽  
Intestinal Calcium Transport

Indirect Inhibition of the Biosynthesis of 1,25-Dihydroxycholecalciferol in Rats Treated with a Diphosphonate

1973 ◽  
Vol 44 (4) ◽  
pp. 335-347 ◽  
Author(s):  
L. F. Hill ◽  
G. A. Lumb ◽  
E. B. Mawer ◽  
S. W. Stanbury
Keyword(s):  
Vitamin D ◽  
Vitamin D3 ◽  
Calcium Transport ◽  
Direct Action ◽  
Intestinal Transport ◽  
Intravenous Dose ◽  
Single Intravenous Dose ◽  
Normal Response ◽  
Intestinal Calcium Transport ◽  
Normal Production

1. Rats treated with disodium ethane-1-hydroxy-1,1-diphosphonate for 14 days developed rickets and impaired intestinal calcium transport, even when receiving large amounts of cholecalciferol (vitamin D3). 2. Vitamin d-deficient rats treated with the diphosphonate, and irrespective of the duration of such treatment, responded initially to a single intravenous dose of cholecalciferol with a normal production of 1,25-dihydroxycholecalciferol. 3. This normal response was followed within 2 days by an apparent inhibition of the renal biosynthesis of 1,25-dihydroxycholecalciferol. It is inferred that the impaired intestinal transport of calcium, in diphosphonate-treated rats receiving vitamin D, is due to a deficiency of this renal metabolite. 4. Inhibition of the synthesis of 1,25-dihydroxycholecalciferol could not be attributed to a direct action of the drug on the renal 1-hydroxylase, but appeared to be determined by the initial normal response to vitamin D. 5. The mechanisms possibly involved in producing this effect are discussed.

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