Risco F, Traba M L
Laboratorio de Bioquímica, Sección de Fisiopatologia Osea, Fundación Jiménez Díaz, Avda Reyes Católicos 2, 28040 Madrid, Spain.
J Physiol Biochem. 2004 Sep;60(3):199-203. doi: 10.1007/BF03167029.
It has been reported that some hypoparathyroid patients with magnesium deficiency showed altered responses to vitamin D treatment. In the same way, in vitro bone studies have demonstrated the existence of a decrease in the 1,25-dihydroxyvitamin D3-induced resorption in bone as a result of magnesium deficiency. These findings suggest some kind of alteration in the 1,25(OH)2D3 in bone in magnesium deficiency. In the present work, using a binding assay based on the 1,25(OH)2D3 and 3H-1,25(OH)2D3 competition for the hormone binding sites in rat calvaria homogenates, a significant decrease in the number of 1,25(OH)2D3 specific binding sites has been found in calvaria incubated in magnesium-deficient medium compared to magnesium-replete ones. Alterations in the hormone-receptor affinity were not found. These results suggest that an alteration in the 1,25(OH)2D3 action on magnesium-deficient bone could be due, at least in part, to a decrease in the number of available vitamin D receptors in bone cells.
据报道,一些患有镁缺乏症的甲状旁腺功能减退患者对维生素D治疗的反应发生了改变。同样,体外骨骼研究表明,由于镁缺乏,1,25 - 二羟基维生素D3诱导的骨吸收减少。这些发现表明,镁缺乏时骨中1,25(OH)2D3存在某种改变。在本研究中,使用基于1,25(OH)2D3和3H - 1,25(OH)2D3竞争大鼠颅骨匀浆中激素结合位点的结合试验,发现在缺镁培养基中孵育的颅骨与镁充足的颅骨相比,1,25(OH)2D3特异性结合位点的数量显著减少。未发现激素 - 受体亲和力的改变。这些结果表明,1,25(OH)2D3对缺镁骨骼作用的改变可能至少部分归因于骨细胞中可用维生素D受体数量的减少。