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Research Article Free access | 10.1172/JCI108815

Role of 1,25-Dihydroxyvitamin D3 on Intestinal Phosphate Absorption in Rats with a Normal Vitamin D Supply

R. Rizzoli, H. Fleisch, and J-P. Bonjour

Department of Pathophysiology, University of Berne, 3010 Berne, Switzerland

Find articles by Rizzoli, R. in: JCI | PubMed | Google Scholar

Department of Pathophysiology, University of Berne, 3010 Berne, Switzerland

Find articles by Fleisch, H. in: JCI | PubMed | Google Scholar

Department of Pathophysiology, University of Berne, 3010 Berne, Switzerland

Find articles by Bonjour, J. in: JCI | PubMed | Google Scholar

Published September 1, 1977 - More info

Published in Volume 60, Issue 3 on September 1, 1977
J Clin Invest. 1977;60(3):639–647. https://doi.org/10.1172/JCI108815.
© 1977 The American Society for Clinical Investigation
Published September 1, 1977 - Version history
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Abstract

In vitamin D-deficient rats, impaired intestinal phosphorus (P) absorption can be corrected by 1,25-dihydroxyvitamin D3[1,25-(OH)2D3]. In the present study, it was investigated whether changes in 1,25-(OH)2D3 production can influence intestinal P transport also in animals with a normal supply of vitamin D. The intestinal P absorption was evaluated in rats using both the in situ duodenal loop technique and the determination of the overall gastrointestinal absorption under three conditions known to influence the production of 1,25-(OH)2D3: (a) variation in dietary P, (b) thyroparathyroidectomy (TPTX) with or without administration of parathyroid hormone (PTH), and (c) treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). In all circumstances changes in duodenal absorption paralleled the changes in the overall fractional absorption. (a) Lowering dietary P stimulated P absorption. (b) TPTX decreased P absorption. This effect was corrected either by the administration of PTH or by the administration of 1,25-(OH)2D3. (c) EHDP, when given at a dose known to inhibit 1,25-(OH)2D3 formation, decreased the duodenal P absorption in both intact and TPTX animals. This effect was corrected by 1,25-(OH)2D3. In the TPTX-EHDP-treated animals, the administration of PTH did not rectify the low duodenal P absorption. These results support the thesis that, in rats with normal vitamin D supply, variations in the endogenous production of 1,25-(OH)2D3 change the rate of P absorption. However, these changes are in such magnitude that they are of relatively small importance when compared to the effect of variation in the dietary intake of P. These results also strongly suggest that the action of PTH on duodenal P transport is mediated by its effect on 1,25-(OH)2D3 production, inasmuch as the effect of the hormone is abolished after blocking the renal 1-hydroxylation with EHDP.

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