Effects of 1,25-dihydroxyvitamin D3 on colonic calcium transport in vitamin D-deficient and normal rats

Abstract

To determine whether prior vitamin D intake influences the intestinal Ca absorptive action of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], the 2 unidirectional transepithelial fluxes of Ca across descending colon segments from rats fed either a vitamin D-deficient or normal diet and injected with either 10, 25 or 75 ng of 1,25(OH)2D3 or vehicle alone were measured in vitro. Vitamin D deficiency abolished net Ca absorption [Jnet, -2 .+-. 2 vs. 12 .+-. 2 (SE) nmol .cntdot. cm-2 .cntdot. h-1, P < 0.001], and 10 ng of 1,25(OH)2D3 raised Jnet to levels found in normal rats. Larger doses (25 and 75 ng) increased Jnet above levels in normal rats given the same dose. In normal rats only 75 ng of 1,25(OH)2D3 increased Ca Jnet above vehicle control values (12 .+-. 2 vs. 38 .+-. 4 nmol .cntdot. cm-2 .cntdot. h-1, P < 0.001). Circulating 1,25(OH)2D3 measured by radioreceptor assay was well correlated with Ca transport. For each dose of 1,25(OH)2D3 higher serum 1,25(OH)2D3 levels were reached in vitamin D-deficient rats. Only the 75-ng dose increased circulating 1,25(OH)2D3 and colonic Ca transport in normal rats. I.v. [3H]-1,25(OH)2D3 disappeared more rapidly from the circulation of normal rats, suggesting that accelerated metabolic degradative processes for 1,25(OH)2D3 may be present in normal, but not in vitamin D-deficient, rats and may account for the lack of a biological response to 1,25(OH)2D3 in normal animals.