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

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

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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