基质细胞外磷酸糖蛋白通过抑制肾小管磷酸盐重吸收导致大鼠出现磷尿症。
Matrix extracellular phosphoglycoprotein causes phosphaturia in rats by inhibiting tubular phosphate reabsorption.
作者信息
Dobbie Hamish, Unwin Robert J, Faria Nuno J R, Shirley David G
机构信息
Department of Physiology and Centre for Nephrology, University College London, Hampstead Campus, Rowland Hill Street, London NW3 2PF, UK.
出版信息
Nephrol Dial Transplant. 2008 Feb;23(2):730-3. doi: 10.1093/ndt/gfm535. Epub 2007 Nov 23.
BACKGROUND
Matrix extracellular phosphoglycoprotein (MEPE), first isolated from tumour-derived tissue from a patient with oncogenic hypophosphataemia, is a putative phosphatonin that has received much less attention than fibroblast growth factor-23. To date, its effect on renal tubular phosphate reabsorption remains undefined.
METHODS
A renal clearance study was performed in anaesthetized rats infused intravenously with a range of doses of MEPE.
RESULTS
MEPE had no effect on glomerular filtration rate (inulin clearance) but caused rapid, dose-dependent increases in absolute and fractional phosphate excretion, wholly attributable to reduced phosphate reabsorption. At a maximal dose, MEPE increased fractional phosphate excretion more than 2-fold, whereas no change was observed in time controls.
CONCLUSION
The results lend support to the hypothesis that MEPE contributes to the phosphaturia of oncogenic hypophosphataemia and of hypophosphataemic rickets.
背景
基质细胞外磷酸糖蛋白（MEPE）最初是从一名致癌性低磷血症患者的肿瘤组织中分离出来的，它是一种假定的磷调节素，受到的关注远少于成纤维细胞生长因子-23。迄今为止，其对肾小管磷重吸收的影响仍不明确。
方法
对麻醉的大鼠进行静脉输注一系列剂量MEPE的肾脏清除率研究。
结果
MEPE对肾小球滤过率（菊粉清除率）无影响，但导致绝对磷排泄量和分数磷排泄量迅速、剂量依赖性增加，这完全归因于磷重吸收减少。在最大剂量时，MEPE使分数磷排泄量增加超过2倍，而在时间对照组中未观察到变化。
结论
这些结果支持了MEPE导致致癌性低磷血症和低磷性佝偻病的磷尿症这一假说。
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