BINDING-PROPERTIES OF GOAT INTESTINAL VITAMIN-D RECEPTORS AS AFFECTEDBY DIETARY CALCIUM AND OR PHOSPHORUS DEPLETION/

Citation
B. Schroder et al., BINDING-PROPERTIES OF GOAT INTESTINAL VITAMIN-D RECEPTORS AS AFFECTEDBY DIETARY CALCIUM AND OR PHOSPHORUS DEPLETION/, Journal of veterinary medicine. Series A, 42(6), 1995, pp. 411-417
Citations number
36
Categorie Soggetti
Veterinary Sciences
ISSN journal
0931184X
Volume
42
Issue
6
Year of publication
1995
Pages
411 - 417
Database
ISI
SICI code
0931-184X(1995)42:6<411:BOGIVR>2.0.ZU;2-1
Abstract
The binding capacity (B-max) and the affinity (K-d) of the intestinal vitamin D receptor (VDR) have been studied using mucosa preparations f rom the duodenum, jejunum and proximal colon of male growing goats whi ch had been kept in a two-factorial (2 x 2) trial on Ca and/or P defic ient diets for 9 weeks. This treatment resulted in significant changes of different parameters of Ca and P homeostasis. Irrespective from th e level of Ca intake, P depletion caused significant hypophosphatemia with corresponding hypercalcemia. In both Ca depleted groups the calci triol concentrations in plasma significantly increased by more than 10 0 % in comparison with normal Ca supply. No changes were recorded for plasma calcitriol concentrations in response to P depletion with an ad equate Ca supply. Plasma PTH levels were only increased significantly in Ca depletion with adequate P supply. Irrespective of different feed ing regimens, the highest B-max values were found in the jejunum. In a ll intestinal segments tested, the B-max values were significantly dec reased by P depletion as compared with an adequate P supply. No effect s on the B-max of VDR were observed in response to changes of Ca suppl y. The K-d values of the VDR were neither affected by different intest inal localizations nor by Ca and/or P depletion. From the present resu lts, it has to be concluded that the physiological relevance of VDR do wn-regulation may not be related to P homeostasis rather than to Ca ho meostasis by minimizing the hypercalcemia induced by P depletion.