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镁补充剂对正常幼鼠骨转换的影响。

Influence of magnesium supplementation on bone turnover in the normal young mouse.

作者信息

Marie P J, Travers R, Delvin E E

出版信息

Calcif Tissue Int. 1983 Sep;35(6):755-61. doi: 10.1007/BF02405119.

DOI:10.1007/BF02405119
PMID:6652550
Abstract

The effect of magnesium (Mg) supplementation on bone metabolism has been studied in the normal young mouse. Weanling male mice were given Mg-supplemented drinking water (5 mM or 32 mM Mg) for 4 weeks. Mineral and skeletal changes were assessed by biochemical methods and by histomorphometric analysis of endosteal bone formation and resorption parameters evaluated on tetracycline double-labeled, undecalcified caudal vertebrae. Magnesium supplementation increased serum and urinary Mg concentrations and bone Mg content. Both the calcification rate and the extent of tetracycline double-labeled osteoid surface increased progressively in Mg-treated mice, whereas the mineralization lag time was shortened. The osteoblastic surface was reduced, leading to a fall in osteoid surface. Stimulation of bone mineralization was associated with a rise in extracellular calcium (Ca) and phosphorus (P) concentrations whereas serum 25-OHD and 1,25(OH)2D levels remained normal. The Mg supplementation increased the number of acid phosphatase stained chondroclasts and osteoclasts and the extent of resorbing surface showing histochemically stained osteoclasts. Although urinary OH-proline increased above normal, Ca, P, and cyclic adenylic acid (cAMP) excretion and phosphate concentration (TmP/GFR) remained normal, suggesting that parathyroid hormone (PTH) secretion was not altered. The trabecular bone volume remained normal, showing that the increased bone resorption was balanced by the stimulated bone mineralization. The results show that Mg supplementation influenced both bone formation and resorption in the young mouse, and that the stimulation of bone mineralization was the result of increased extracellular mineral availability.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在正常的幼年小鼠中研究了补充镁(Mg)对骨代谢的影响。给断奶的雄性小鼠饮用补充了镁的水(5 mM或32 mM Mg),持续4周。通过生化方法以及对四环素双标记、未脱钙的尾椎骨进行骨内膜骨形成和吸收参数的组织形态计量分析来评估矿物质和骨骼变化。补充镁可提高血清和尿液中的镁浓度以及骨镁含量。在镁处理的小鼠中,钙化率和四环素双标记类骨质表面的范围均逐渐增加,而矿化延迟时间缩短。成骨细胞表面减少,导致类骨质表面下降。骨矿化的刺激与细胞外钙(Ca)和磷(P)浓度的升高相关,而血清25-OHD和1,25(OH)2D水平保持正常。补充镁增加了酸性磷酸酶染色的软骨破骨细胞和破骨细胞的数量以及显示组织化学染色破骨细胞的吸收表面范围。尽管尿羟脯氨酸高于正常水平,但钙、磷和环磷酸腺苷(cAMP)排泄以及磷酸盐浓度(TmP/GFR)保持正常,表明甲状旁腺激素(PTH)分泌未改变。小梁骨体积保持正常,表明增加的骨吸收被刺激的骨矿化所平衡。结果表明,补充镁影响了幼年小鼠的骨形成和吸收,并且骨矿化的刺激是细胞外矿物质可用性增加的结果。(摘要截短为250字)

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本文引用的文献

1
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Effect of magnesium deficiency on rat bone and kidney sensitivity to parathyroid hormone.镁缺乏对大鼠骨骼和肾脏对甲状旁腺激素敏感性的影响。
Calcif Tissue Int. 1985 May;37(3):268-75. doi: 10.1007/BF02554873.
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Effects of magnesium and lactose supplementation on bone metabolism in the X-linked hypophosphatemic mouse.补充镁和乳糖对X连锁低磷血症小鼠骨代谢的影响。
Metabolism. 1983 Feb;32(2):165-71. doi: 10.1016/0026-0495(83)90224-x.
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Calcium homeostasis and bone pathology in magnesium deficient rats.镁缺乏大鼠的钙稳态与骨骼病理学
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Continuous infusion of 1,25-dihydroxyvitamin D3 stimulates bone turnover in the normal young mouse.持续输注1,25 - 二羟维生素D3可刺激正常幼鼠的骨转换。
Calcif Tissue Int. 1983 Jul;35(4-5):418-25. doi: 10.1007/BF02405070.
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Bone response to phosphate and vitamin D metabolites in the hypophosphatemic male mouse.低磷血症雄性小鼠骨骼对磷酸盐和维生素D代谢物的反应
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Effect of vitamin D sterols and dietary magnesium on calcium and phosphorous homeostasis.维生素D甾醇和膳食镁对钙磷稳态的影响。
Am J Physiol. 1981 Jul;241(1):E35-41. doi: 10.1152/ajpendo.1981.241.1.E35.
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Serum 1,25-dihydroxyvitamin D concentration in hypophosphatemic vitamin D-resistant rickets.低磷性维生素D抵抗性佝偻病患者的血清1,25-二羟维生素D浓度
Calcif Tissue Int. 1981;33(2):173-5. doi: 10.1007/BF02409431.