Action ofSolanum Malacoxylonon Intestinal Calcium Transport in Vitamin D-Deficient-Prednisolone Treated Rats

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Abstract
The daily administration of 20 mg/kg of prednisolone, during 10 days to rats on a vitamin D-free normal calcium diet, inhibited the hypercalcemic action and diminished the stimulatory effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) upon the intestinal transport of calcium assessed by the everted gut sac technique. On the other hand, the administration of Solanum malacoxylon (SM) increased serum calcium and intestinal calcium transport in rats on a normal calcium diet either treated or not treated with prednisolone. The administration of prednisolone to rats on a vitamin D and calcium-deficient diet reduced the stimulating effect of both 1,25(OH)2D3 and SM upon intestinal calcium transport. However the hypercalcemic effect of SM was preserved whereas that of 1,25(OH)2D3 was abolished. Prednisolone treatment to vitamin D-deficient rats produced a significant decrease of plasma phosphorus and inhibited the hyperphosphatemic effect of all vitamin D derivatives. These results suggest that the calcinogenic factor of SM is not identical to 1,25(OH)2D3 and is not therefore rapidly degraded in the intestinal cells as 1,25(OH)2D3. Alternatively, the sugar molecules attached to the steroid compound in SM would prevent its rapid liberation; thus, the intestinal cells would be continuously exposed to small quantities of the steroid 1,25(OH)2D3 that could act before metabolic degradation. Similarly, the slow transformation of 25-hydroxyvitamin D3 (25(OH)D3) in 1,25(OH)2D3 would explain the persistance of 25(OH)D3 actions in situations where 1,25(OH)2D3 is inactive.