1,25-Dihydroxyvitamin D3Modulates Glucocorticoid-Induced Alteration in Serum Bone Gla Protein and Bone Histomorphometry
- 1 February 1987
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 120 (2) , 531-536
- https://doi.org/10.1210/endo-120-2-531
Abstract
Glucocorticoid excess is associated with alterations in the vitamin D endocrine system. The aim of this study was to assess change in serum bone Gla protein (BGP) after low and high dose cortisone acetate treatment and to assess whether these alterations are altered or attenuated by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] administration. Five groups of rats were studied and compared to a control group [cortisone acetate in doses of 0.2, 3.3, and 5.0 mg/100 g BW; 1,25-(OH)2D3 in a dose of 100 ng/100 g BW; and a combination of 1,25-(OH)2D3 (100 ng/100 g BW) plus cortisone acetate (3.3 mg/100 g BW)]. Each animal received daily sc injections for 27 days. BGP decreased significantly by day 7 in the two groups receiving high doses of cortisone acetate compared to control group values (65.20 .+-. 4.38 vs. 150.18 .+-. 6.13 ng/ml in the intermediate dose group and 91.57 .+-. 5.30 vs. 150.18 .+-. 6.13 ng/ml in the high dose group; P < 0.01); this effect persisted until day 28. Histomorphometry revealed decreased formation and resorption in the two high dose cortisone acetate groups, whereas low dose cortisone acetate produced no histological change. The combination therapy lessens any change in BGP until day 28 when BGP was lower than the control value (P < 0.01); histomorphometry showed that combination therapy prevents the effect of cortisone acetate by increasing bone formation and resorption. The data demonstrate that high doses of cortisone acetate suppress bone formation and that this is reflected in the low serum BGP values. Thus, BGP may be a marker of glucocorticoid-induced bone disease. 1,25-(OH)2D3 protects against glucocorticoid-induced bone disease and the normal BGP level reflects this.This publication has 14 references indexed in Scilit:
- The renal metabolism of 25-hydroxyvitamin D3 in the rat: Regulation by 1,25-dihydroxyvitamin D3Calcified Tissue International, 1983
- Glucocorticoid regulation of 1,25(OH)2-vitamin D3 receptors in cultured mouse bone cells.Journal of Biological Chemistry, 1982
- Quantitation of vitamin D and its metabolites and their plasma concentrations in five species of animalsAnalytical Biochemistry, 1981
- New biochemical marker for bone metabolism. Measurement by radioimmunoassay of bone GLA protein in the plasma of normal subjects and patients with bone disease.Journal of Clinical Investigation, 1980
- Absence of the vitamin K-dependent bone protein in fetal rat mineral. Evidence for another gamma-carboxyglutamic acid-containing component in bone.Journal of Biological Chemistry, 1980
- Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.Journal of Clinical Investigation, 1979
- REDUCTION OF SERUM-1,25-DIHYDROXYVITAMIN-D3 IN CHILDREN RECEIVING GLUCOCORTICOIDSThe Lancet, 1978
- Intestinal Calcium Absorption in Exogenous HypercortisonismJournal of Clinical Investigation, 1977
- Cartilage Sulfation and Serum Somatomedin in Rats During and After Cortisone-Induced Growth ArrestEndocrinology, 1976
- Characterization of a gamma-carboxyglutamic acid-containing protein from bone.Proceedings of the National Academy of Sciences, 1976