The relationship between vitamin D-stimulated calcium transport and intestinal calcium-binding protein in the chicken
- 15 January 1978
- journal article
- research article
- Published by Portland Press Ltd. in Biochemical Journal
- Vol. 170 (1) , 93-101
- https://doi.org/10.1042/bj1700093
Abstract
The rapid stimulation of intestinal Ca2+ 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 Ca-binding protein synthesis. By 1 h after a dose of 125 ng of 1,25-dihydroxycholecalciferol Ca2+ transport is increased. This is at least 2 h before Ca-binding protein can be detected immunologically and 1 h before synthesis of the protein begins on polyribosomes, and thus the hormone stimulates Ca2+ transport before Ca-binding-protein biosynthesis is induced. The maximum increase in Ca2+ transport observed after this dose of 1,25-dihydroxycholecalciferol (attained by 8 h) is similar to that observed after 1.25-25 .mu.g 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 Ca2+ transport has declined to its basal rate, the cellular content of calcium-binding protein remains elevated. Ca-binding protein is synthesized on free rather than membrane-bound polyribosomes, which implies that it is an intracellular protein. Rachitic chicks require the presence of dietary Ca for maximum stimulation of Ca-binding protein production by cholecalciferol. Ca-binding protein is apparently an intracellular protein, and its synthesis may be a consequence of the raised intracellular Ca content of the intestinal epithelial cells resulting from 1,25-dihydroxycholecalciferol-stimulated Ca2+ transport. Ca-binding-protein synthesis may be necessary for maintaining the stimulated rate of Ca2+ transport, which is initiated by other factors.This publication has 25 references indexed in Scilit:
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