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Biomedical subjects

H F DeLuca

Publications and source records attributed to H F DeLuca.

At least 703 records · Page 39Linked to original sources
PubMed1969

Vitamin D3-stimulated template activity of chromatin from rat intestine.

Administration of vitamin D to rats deficient in this vitamin markedly increases the template activity for DNA-dependent RNA synthesis by rat intestinal mucosal chromatin. The maximum stimulation of template activity occurs three hours after a dose of 2000 international units of vitamin D(3) is given. These results support the concept that vitamin D functions by initiating the transcription of DNA into mRNA, which codes for functional protein(s) involved in calcium transport in the small intestine.

Adenosine Triphosphate↗
PubMed1969

The role of the liver in the metabolism of vitamin D.

The metabolism of vitamin D(3) has been studied after intravenous injection of 10 IU of [1,2-(3)H]-vitamin D(3) to vitamin D-deficient rats. The disappearance of the radioactivity from the plasma follows a very peculiar pattern characterized by an early rapid disappearance followed by a rebound of radioactivity before assuming still a third rather slow disappearance rate. The "rebound" phenomenon is concomitant with a rapid release of the radioactivity from the liver and is accounted for by the appearance of 25-hydroxycholecalciferol and other metabolites in the blood. It is postulated that the liver is the major site of transformation of vitamin D(3) into 25-hydroxycholecalciferol.

Animals↗
PubMed1969

"Activation" of vitamin D by the liver.

Isolation of the liver from the circulation of rats eliminates almost completely their ability to convert [1,2]-(3)H vitamin D(3) into its biologically active metabolite, 25-hydroxycholecalciferol, as well as certain other metabolites. It is concluded that the liver is the major if not the only physiologic site of hydroxylation of vitamin D(3) (cholecalciferol) into 25-hydroxycholecalciferol. The osteodystrophy and the higher requirements for vitamin D observed in hepatic insufficiencies may be due to an inability of the liver to transform vitamin D into its metabolically active form.

Animals↗