Influence of Dietary Vitamin D3on the Circulating Concentration of its Active Metabolites in the Chick and Rat

Publisher Website
Google Scholar
Abstract
Plasma concentrations of 25-hydroxyvitamin D3 (25-OHD3) and 1.alpha.,25-dihydroxyvitamin D3 (1.alpha.,25-(OH)2D3) in growing chicks and weanling rats were measured by a new radioreceptor assay to determine the effects of varying dietary levels of vitamin D3. The plasma concentration of 25-OHD3 fell from 14.1 ng/ml in 1 day old chicks to undetectable levels after 3 wk on a rachitogenic diet. Circulating 1.alpha.,25-(OH)2D3 hormone also decreased from 8.9 ng/100 ml to undetectable levels at 3 wk in these chicks. Chicks receiving an optimal supplement of vitamin D3 (1.4 IU/g diet) for 3-4 wk had plasma 25-OHD3 and 1.alpha.,25-(OH)2D3 levels of 21-35 ng/ml and 5.1-7.5 ng/100 ml, respectively. Nutritional supplementation with a 50-fold excess of vitamin D3 (70 IU/g diet) elicited a substantial increase in plasma 25-OHD3 to 87-130 ng/ml, while plasma 1.alpha.,25-(OH)2D3 was not increased. Increasing dietary Ca from 1.4-2.8% did not alter the circulating level of vitamin D3 metabolites in chicks fed 1.4 IU of vitamin D3/g diet. Direct measurement of the renal 25-OHD3-1.alpha.-hydroxylase, in vitro, showed that lowering dietary Ca or exclusion of vitamin D3 stimulated the biosynthesis of 1.alpha.,25-(OH)2D3, but raising Ca did not alter the enzyme activity. The circulating concentration of the 1.alpha.,25-(OH)2D3 hormone in the chick is probably unaffected by abnormally high intakes of vitamin D3 or Ca, but the renal production of the hormone increases during vitamin D3 or Ca deprivation. Additional studies in rats fed a diet supplemented with either 2 or 1000 IU of vitamin D3/g verify that the circulating concentration of 25-OHD3 is markedly increased when the dietary intake of vitamin D3 is elevated. 1.alpha.,25-(OH)2D3 is not increased under these conditions, but actually falls significantly when the dietary level of vitamin D3 is raised from 2 to 1000 IU/g. These studies in both the chick and rat indicate that dietary vitamin D3 excess enhances circulating 25-OHD3, probably because the vitamin D3-25-hydroxylase enzyme is not stringently controlled. The fact that the circulating 1.alpha.,25-(OH)2D3 is not concomitantly increased may reflect either decreased synthesis or increased utilization of the 1.alpha.,25-(OH)2D3 sterol.

This publication has 1 reference indexed in Scilit: