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H F DeLuca

Publications and source records attributed to H F DeLuca.

At least 649 records · Page 36Linked to original sources
PubMed1972

1,25-dihydroxycholecalciferol: metabolite of vitamin D3 active on bone in anephric rats.

Nephrectomy prevents completely the bone calcium mobilization response to 25-hydroxycholecalciferol. In contrast it does not prevent this response to 1,25-dihydroxycholecalciferol. Because it is known that the kidney is the site of 1,25-dihydroxycholecalciferol formation, these results provide evidence that 1,25-dihydroxycholecalciferol or a further metabolite thereof and not 25-hydroxycholecalciferol is the metabolically active form of vitamin D(3) responsible for bone calcium mobilization.

Animals↗
PubMed1972

1,25-dihydroxycholecalciferol: a potent stimulator of bone resorption in tissue culture.

1,25-Dihydroxycholecalciferol (DHCC), isolated from kidney homogenates incubated with 25-hydroxycholecalciferol (HCC), stimulated the release of previously incorporated (45)45Ca from fetal rat bones in organ culture, at concentrations of 10(-10) to 10(-8)M. The dose response curves for 1,25-DHCC and 25-HCC, the parent compound, are parallel, but 1,25-DHCC is about 100 times as potent on a weight basis. Brief exposure to maximum doses of either agent leads to prolonged bone resorption.

Animals↗
PubMed1972

Metabolism of 1,25-dihydroxycholecalciferol in the rat.

Administration of 60 pmoles of 1,25-dihydroxycholecalciferol to vitamin D-deficient rats on a low calcium diet gives a maximal intestinal calcium transport response in 7 hr and a maximal bone calcium mobilization response in 12 hr. During the 48 hr after injection of radioactive 1,25-dihydroxycholecalciferol, unchanged 1,25-dihydroxycholecalciferol accounts for 71-98% of the radioactivity found in the intestine with minor amounts appearing in more polar metabolites. In the bone, for the 1st 12 hr, 1,25-dihydroxycholecalciferol is the major form (75-82%) present while at 24 hr, the amount of 1,25-dihydroxycholecalciferol decreases with a corresponding rise in the amounts of metabolites both less polar and more polar than the 1,25-dihydroxycholecalciferol. Since these metabolies are at their highest concentration when bone calcium mobilization is decreasing, they are most likely not responsible for the calcium mobilization observed during the 1st 12 hr. The appearance of water-soluble radioactivity in the kidney, plasma, liver, and muscle 24 hr after 1,25-dihydroxycholecalciferol injection has been demonstrated. The present results suggest that, although 1,25-dihydroxycholecalciferol is converted to further metabolites in the rat, it is probably the form of vitamin D responsible for initiating intestinal calcium transport and bone calcium mobilization.

Animals↗
PubMed1971

Strontium induced rickets: metabolic basis.

Dietary strontium inhibits both the synthesis of 1,25-dihydroxycholecalciferol and intestinal calcium absorption in vitamin D(3)-repleted chicks. 1,25-Dihydroxycholecalciferol restores calcium absorption to normal, while 25-hydroxycholecalciferol is without effect in the strontium-fed chick. It is suggested that strontium induces rickets by blocking the biosynthesis of 1,25-dihydroxycholecalciferol, the metabolically active form of vitamin D in the intestine.

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