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Hector F. DeLuca, PhD; Louis V. Avioli, MD

Arch Intern Med. 1970;126(5):896-899.

Abstract
Vitamin D₃ is converted by a liver enzyme system, calciferol-25-hydroxylase, to 25-hydroxycholecalciferol (25-HCC), the active hormonal form of the vitamin. This hydroxylase is feedback inhibited by 25-HCC, and probably represents an important physiologic control step for active vitamin D. The 25-HCC is further converted in intestine, kidney, and bone to two more polar metabolites which probably represent the metabolically active form of vitamin D₃. Evidence has been presented that in uremia, excessive metabolism of vitamin D results in low plasma levels of 25-HCC. In chronically uremic rats, 25-HCC is at least one hundredfold more effective than vitamin D₃ in restoring calcium absorption. In uremics, treatment with 10,000 international units (IU) of 25-HCC/day, improves calcium absorption, increases urinary and plasma calcium and decreases plasma alkaline phosphatase. Thus, 25-HCC may be the drug of choice in bone disease of uremia.

Author Affiliations
Madison, Wis; St. Louis

From the Department of Biochemistry, University of Wisconsin, Madison (Dr. DeLuca) and the Department of Medicine, Washington University, St. Louis (Dr. Avioli).

Footnotes
Received for publication July 8, 1970; accepted July 20.

Read before the session entitled "Mineral Metabolism" (Hillel J. Gitelman, MD, chairman) of the Symposium on Uremic Toxins sponsored by the National Institute of Arthritis and Metabolic Diseases, Monterey, Calif, March 20, 1970.

Reprint requests to Department of Biochemistry, University of Wisconsin, Madison 53706 (Dr. DeLuca).

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