Osteopenia following total gastrectomy in the rat--state of mineral metabolism and bone histomorphometry.
Osteopenia following total gastrectomy in the rat--state of mineral metabolism and bone histomorphometry.
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大鼠全胃切除术后骨质减少——矿物质代谢和骨组织形态计量学状态。
DOI：
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
Werner Hohenberger
中科院分区：
文献类型：
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作者：
G. Rümenapf;P. Schwille;Reinhold G. Erben;M. Schreiber;W. Fries;A. Schmiedl;Werner Hohenberger
在人类的全胃切除术(GX)之后，经常会出现骨量减少，但具体情况尚不清楚。目前对大鼠的研究旨在阐明其发病机制。GX后17周，我们评估了钙、镁和磷的代谢以及骨参数，包括基于荧光色素的骨组织形态计量学。GX大鼠粪便镁含量增加，但肠道对磷、钙、镁的吸收在正常范围内，尿钙、镁、羟脯氨酸和吡啶交联物的排泄也在正常范围内。相反，尿磷和环磷酸腺苷均显著升高。GX大鼠血清胃泌素和25-羟基维生素D(25-OHD)降低，钙、镁、磷、甲状旁腺激素(PTH)、降钙素和骨钙素正常，1，25-二羟基维生素D[1，25(OH)2D]显著升高。GX大鼠骨密度和矿物质含量显著降低，高转换性骨量减少严重，类骨质宽度正常但成骨时间明显缩短，骨形成率增加，破骨细胞数量增加。我们的结论是，在GX(1)后，存在高周转性骨量减少，矿化正常，其他组织形态计量学特征类似于高磷尿症和随后的高维生素D症状态；(2)正常的血清PTH水平和几个间接的甲状旁腺功能指标与(继发性)甲状旁腺功能亢进症的存在相抵触，而由于1，25(OH)2D升高而导致的骨动员增加解释了以牺牲骨矿物质为代价维持血清矿物质，尤其是钙的动态平衡；(3)存在复杂的矿物质代谢效应因素，其中低25-OHD-PTH独立的肾脏磷酸盐丢失和高1，25(OH)2D是显著特征。本实验所建立的动物模型可用于该领域的进一步研究。
Total gastrectomy (GX) in humans is frequently followed by osteopenia, but the details are unclear. The present investigations in the rat were aimed at elucidating its pathogenesis. Seventeen weeks after GX, we evaluated Ca, Mg and P metabolism as well as bone parameters, including fluorochrome-based bone histomorphometry. In GX rats, fecal Mg was increased, but intestinal absorption of P, Ca, and Mg was within normal limits, as was the urinary excretion of Ca, Mg, hydroxyproline and the pyridinium cross-links. In contrast, urinary P as well as cyclic AMP were significantly increased. In serum of GX rats, gastrin and 25-hydroxyvitamin D (25-OHD) were decreased, and Ca, Mg, P, parathyroid hormone (PTH), calcitonin, and the bone marker osteocalcin were normal, whereas 1,25-dihydroxyvitamin D [1,25(OH)2D] was significantly increased. GX rats had significantly reduced bone density and mineral content, severe high-turnover osteopenia, characterized by normal width but significantly decreased maturation time of osteoid, increased bone formation rate, and increased numbers of osteoclasts. We concluded that after GX (1) there is high-turnover osteopenia with normal mineralization and other histomorphometric features resembling those seen in states with hyperphosphaturia and subsequent hypervitaminosis D; (2) normal serum PTH levels and several indirect indicators of parathyroid gland function argue against the presence of (secondary) hyperparathyroidism, whereas increased bone mobilization due to elevated 1,25(OH)2D explains the maintenance of homeostasis of serum minerals, especially Ca, at the expense of bone mineral; (3) a complex interplay of mineral-metabolic effectors exists, among which low 25-OHD-PTH-independent renal phosphate losses, and high 1,25(OH)2D are prominent features. The presented animal model is recommended for future research in this area.