Indirect Inhibition of the Biosynthesis of 1,25-Dihydroxycholecalciferol in Rats Treated with a Diphosphonate
| Autor: | E. B. Mawer, S. W. Stanbury, L. F. Hill, G. A. Lumb |
|---|---|
| Rok vydání: | 1973 |
| Předmět: |
Vitamin
Drug medicine.medical_specialty Duodenum media_common.quotation_subject Metabolite Organophosphonates Biological Transport Active chemistry.chemical_element Rickets Calcium Kidney Tritium Bone and Bones chemistry.chemical_compound Biosynthesis Internal medicine medicine Vitamin D and neurology Animals Urea Cholecalciferol media_common Chromatography Spectrophotometry Atomic Phosphorus General Medicine medicine.disease Rats Endocrinology chemistry |
| Zdroj: | Clinical Science. 44:335-347 |
| ISSN: | 0301-0538 |
| DOI: | 10.1042/cs0440335 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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