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Bone specific binding sites for 1,25(OH)2D3 in magnesium deficiency
1Laboratorio de Bioquímica, Sección de Fisiopatologia Osea, Fundación Jiménez Díaz, Avda Reyes Católicos 2, 28040 Madrid, Spain.
Journal of Physiology and Biochemistry
|February 11, 2005
Summary
Magnesium deficiency reduces vitamin D receptors in bone, impairing 1,25-dihydroxyvitamin D3 action. This finding explains altered vitamin D treatment responses in hypoparathyroid patients with low magnesium levels.
Area of Science:
- Endocrinology
- Bone Biology
- Mineral Metabolism
Background:
- Hypoparathyroidism and magnesium deficiency can alter vitamin D treatment responses.
- Magnesium deficiency is linked to reduced 1,25-dihydroxyvitamin D3-induced bone resorption in vitro.
- These observations suggest impaired vitamin D action in bone during magnesium deficiency.
Purpose of the Study:
- To investigate the effect of magnesium deficiency on vitamin D receptors in bone.
- To determine if magnesium deficiency alters the number or affinity of 1,25-dihydroxyvitamin D3 binding sites in bone cells.
Main Methods:
- Utilized a competitive binding assay using 1,25-dihydroxyvitamin D3 and radiolabeled 3H-1,25-dihydroxyvitamin D3.
- Assayed hormone binding sites in rat calvaria homogenates.
- Compared calvaria incubated in magnesium-deficient versus magnesium-replete media.
Main Results:
- A significant decrease in the number of specific 1,25-dihydroxyvitamin D3 binding sites was observed in magnesium-deficient bone.
- No alterations in hormone-receptor affinity were detected.
- The reduction in binding sites suggests impaired vitamin D signaling.
Conclusions:
- Magnesium deficiency leads to a reduced number of vitamin D receptors in bone cells.
- This decrease in receptor availability likely contributes to the altered action of 1,25-dihydroxyvitamin D3 on bone in magnesium-deficient states.
- Findings may explain clinical observations in hypoparathyroid patients with magnesium deficiency.