To determine whether prior vitamin D intake influences the intestinal calcium absorptive action of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], we measured in vitro the two unidirectional transepithelial fluxes of calcium 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. Vitamin D deficiency abolished net calcium absorption [J(net), -2 ± 2 vs. 12 ± 2 (SE) nmol.cm-2.h-1, P < 0.001], and 10 ng of 1,25(OH)2D3 raised J(net) to levels found in normal rats. Larger doses (25 and 75 ng) increased J(net) above levels in normal rats given the same dose. In normal rats only 75 ng of 1,25(OH)2D3 increased calcium J(net) above vehicle control values (12 ± 2 vs. 38 ± 4 nmol.cm2.h-1, P < 0.001). Circulating 1,25(OH)2D3 measured by radioreceptor assay was well correlated with calcium 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 calcium transport in normal rats. Intravenous [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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|State||Published - Jan 1 1984|
ASJC Scopus subject areas
- Physiology (medical)