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Research Article Free access | 10.1172/JCI105605
Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
Department of Medicine, Jewish Hospital of St. Louis, St. Louis, Mo.
Department of Biochemistry, University of Wisconsin, Madison, Wisc.
†Career Research Development awardee (6-K3-GM-22-676-03).
*Submitted for publication December 6, 1966; accepted March 6, 1967.
Supported in part by grants AM06404 and AM11247 from the National Institute of Arthritis and Metabolic Diseases.
Find articles by Avioli, L. in: JCI | PubMed | Google Scholar
Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
Department of Medicine, Jewish Hospital of St. Louis, St. Louis, Mo.
Department of Biochemistry, University of Wisconsin, Madison, Wisc.
†Career Research Development awardee (6-K3-GM-22-676-03).
*Submitted for publication December 6, 1966; accepted March 6, 1967.
Supported in part by grants AM06404 and AM11247 from the National Institute of Arthritis and Metabolic Diseases.
Find articles by Lee, S. in: JCI | PubMed | Google Scholar
Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
Department of Medicine, Jewish Hospital of St. Louis, St. Louis, Mo.
Department of Biochemistry, University of Wisconsin, Madison, Wisc.
†Career Research Development awardee (6-K3-GM-22-676-03).
*Submitted for publication December 6, 1966; accepted March 6, 1967.
Supported in part by grants AM06404 and AM11247 from the National Institute of Arthritis and Metabolic Diseases.
Find articles by McDonald, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
Department of Medicine, Jewish Hospital of St. Louis, St. Louis, Mo.
Department of Biochemistry, University of Wisconsin, Madison, Wisc.
†Career Research Development awardee (6-K3-GM-22-676-03).
*Submitted for publication December 6, 1966; accepted March 6, 1967.
Supported in part by grants AM06404 and AM11247 from the National Institute of Arthritis and Metabolic Diseases.
Find articles by Lund, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
Department of Medicine, Jewish Hospital of St. Louis, St. Louis, Mo.
Department of Biochemistry, University of Wisconsin, Madison, Wisc.
†Career Research Development awardee (6-K3-GM-22-676-03).
*Submitted for publication December 6, 1966; accepted March 6, 1967.
Supported in part by grants AM06404 and AM11247 from the National Institute of Arthritis and Metabolic Diseases.
Find articles by DeLuca, H. in: JCI | PubMed | Google Scholar
Published June 1, 1967 - More info
Vitamin D3-3H has been administered intravenously to seven normal subjects, three patients with biliary fistulas, and four patients with cirrhosis. Plasma D3-3H half-times normally ranged from 20 to 30 hours. in vivo evidence that a metabolic transformation of vitamin D occurs was obtained, and a polar biologically active vitamin D metabolite was isolated from plasma.
Urinary radioactivity averaged 2.4% of the administered dose for the 48-hour period after infusion, and all the excreted radioactivity represented chemically altered metabolites of vitamin D. The metabolites in urine were mainly water-soluble, with 26% in conjugated form.
From 3 to 6% of the injected radioactivity was excreted in the bile of subjects with T-tube drainage and 5% in the feces of patients having no T-tube. The pattern of fecal and biliary radioactivity suggested that the passage of vitamin D and its metabolites from bile into the intestine represents an essential stage for the fecal excretion of vitamin D metabolites in man.
Abnormally slow plasma disappearance of vitamin D3-3H in patients with cirrhosis was associated with a significant decrease in the quantity and rate of glucuronide metabolite excretion in the urine.