The relationship between vitamin D-stimulated calcium transport and intestinal calcium-binding protein in the chicken

Abstract

1. The rapid stimulation of intestinal Ca(2+) transport observed in vitamin D-deficient chicks after receiving 1,25-dihydroxycholecalciferol has necessitated a re-evaluation of the correlation hitherto observed between this stimulation and the induction of calcium-binding protein synthesis. By 1h after a dose of 125ng of 1,25-dihydroxycholecalciferol, Ca(2+) transport is increased. This is at least 2h before calcium-binding protein can be detected immunologically and 1h before synthesis of the protein begins on polyribosomes, and thus the hormone stimulates Ca(2+) transport before calcium-binding-protein biosynthesis is induced. 2. The maximum increase in Ca(2+) transport observed after this dose of 1,25-dihydroxycholecalciferol (attained by 8h) is similar to that observed after 1.25-25mug of cholecalciferol, but the stimulation is only short-lived, in contrast with the effect observed after the vitamin. At later times after the hormone, however, when Ca(2+) transport has declined to its basal rate, the cellular content of calcium-binding protein remains elevated. 3. Calcium-binding protein is synthesized on free rather than membrane-bound polyribosomes, which implies that it is an intracellular protein. 4. Rachitic chicks require the presence of dietary calcium for maximum stimulation of calcium-binding protein production by cholecalciferol. 5. These results suggest that calcium-binding protein is an intracellular protein, and that its synthesis may be a consequence of the raised intracellular calcium content of the intestinal epithelial cells resulting from 1,25-dihydroxycholecalciferol-stimulated Ca(2+) transport. We propose that calcium-binding-protein synthesis is necessary for maintaining the stimulated rate of Ca(2+) transport, which is initiated by other factors.

Evidence for multiple effects of vitamin D3 on calcium absorption: response of rachitic chicks, with or without partial vitamin D3 repletion, to 1,25-dihydroxyvitamin D3.

“…The protein synthesis theory of 1,25(OH)2D3 function has been questioned recently (9,10,12) (10,13,14). However, this lack oftemporal correspondence has never been observed in this laboratory when truly vitamin Ddeficient chicks were used (Fig.…”

“…The primary effect of D3 was considered to be a modification of membrane phospholipids and thereby an increase in the permeability of the brush border membrane to Ca2+, with subsequent steps in the absorption ofcalcium somewhat secondary to this event (11,12). In this vein, Spencer et al (13), Bikle et al (10), and Thomasset et aL (14) reported that the administration of a single dose of 1,25(OH)2D3 to vitamin D-deficient animals stimulates calcium absorption prior to the induction of the synthesis of calciumbinding protein (CaBP), a protein product ofthe genomic action of the 1,25(OH)2D3. However, this lack of temporal correlation between CaBP synthesis and 1,25(OH)2D3-stimulated calcium absorption is contrary to our experience, as documented in this report.…”

Cholecalcin (a 9‐kDa cholecalciferol‐induced calcium‐binding protein) messenger RNA

“…Previous studies using an in vitro translation assay [36] showed that mRNA coding for 28-kDa cholecalcin appears in the chick intestine 2 h after a single calcitriol dose administered to vitamin-Ddeficient birds. The relatively low yield of 28-kDa cholecalcin in the cell-free system compared with that of the 9-kDa protein [14,37] may account for the difference between the short delay for 9-kDa-cholecalcin mRNA stimulation and the later 28-kDa-cholecalcin mRNA induction. However, the changes in the concentrations of both 9-kDa cholecalcin and its mRNA were dissociated in the period immediately following hormonal induction (Fig.…”

Purification and characterization of spermidine N1‐acetyltransferase from chick duodenum

“…Ornithine decarboxylase (EC 4.1.1.17), spermidine N ' -acetyltransferase (EC 2.3.1.57), polyamine oxidase (EC 1.4.3.6). transport activity apparently preceded the synthesis of calbindin [20,25,261. The role of calbindin in the intestinal calcium transport mechanism is still a matter of controversy.…”