Plasma concentrations of 25-hydroxy-vitamin D 3 (25-OHD 3) and 1α,25-dihydroxyvitamin D 3 (1α,25-(OH) 2D 3) in growing chicks and weanling rats were measured by a new radioreceptor assay to determine the effects of varying dietary levels of vitamin D 3. The plasma concentration of 25-OHD 3 fell from 14.1 ng/ml in 1-day-old chicks to undetectable levels after 3 weeks on a rachitogenic diet. Circulating 1α,25-(OH) 2D 3 hormone also decreased from 8.9 ng/100 ml to undetectable levels at 3 weeks in these chicks. Chicks receiving an optimal supplement of vitamin D 3 (1.4 IU/g diet) for three to four weeks had plasma 25-OHD 3 and 1α,25-(OH) 2D 3 levels of 21-35 ng/ml and 5.1-7.5 ng/100 ml, respectively. Nutritional supplementation with a 50-fold excess of vitamin D 3 (70 IU/g diet) elicited a substantial increase in plasma 25-OHD 3 to 87-130 ng/ml, while plasma 1α,25-(OH) 2D 3 was not increased. Increasing dietary calcium from 1.4 to 2.8% did not alter the circulating level of vitamin D 3 metabolites in chicks fed 1.4 IU of vitamin D 3/g diet. Direct measurement of the renal 25-OHD 3-1α-hydroxylase, in vitro, showed that lowering dietary calcium or exclusion of vitamin D 3 stimulated the biosynthesis of 1α,25-(OH) 2D 3, but raising calcium did not alter the enzyme activity. It is concluded that the circulating concentration of the 1α,25-(OH) 2D 3 hormone in the chick is unaffected by abnormally high intakes of vitamin D 3 or calcium, but the renal production of the hormone increases during vitamin D 3 or calcium deprivation. Additional studies in rats fed a diet supplemented with either 2 or 1000 IU of vitamin D 3/g verify that the circulating concentration of 25-OHD 3 is markedly increased when the dietary intake of vitamin D 3 is elevated. Moreover, 1α,25-(OH) 2D 3 is not increased under these conditions, but actually falls significantly when the dietary level of vitamin D 3 is raised from 2 to 1000 IU/g. These studies in both the chick and rat indicate that dietary vitamin D 3 excess enhances circulating 25-OHD 3, probably because the vitamin D 3-25-hydroxylase enzyme is not stringently controlled. The fact that the circulating 1α,25-(OH) 2D 3 is not concomitantly increased may reflect either decreased synthesis or increased utilization of the 1α,25-(OH) 2D 3 sterol.
|Original language||English (US)|
|Number of pages||8|
|Publication status||Published - 1977|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism