Teschner M, Paczek L, Schaefer R M, Heidland A
Department of Nephrology, University of Würzburg, FRG.
Miner Electrolyte Metab. 1992;18(2-5):89-91.
The obese Zucker rat develops non-immune-mediated spontaneous focal glomerulosclerosis. Mesangial matrix expansion is an important initiating hallmark of such glomerular damage and fibronectin is a normal constituent of mesangial extracellular matrix. Using a quantitative method based on enzyme immunoassay, we have assessed the intraglomerular fibronectin content and its degradation in obese Zucker rats and their lean littermates. In the obese Zucker rats the glomerular fibronectin content was significantly higher than in the control animals. Furthermore, proteinase activity against fibronectin was significantly reduced in the glomeruli of obese Zucker rats compared to the control animals. These data demonstrate that in obese Zucker rats there is a glomerular accumulation of fibronectin which we propose is at least partly due to diminished proteolytic digestion. We speculate that this result might indicate a possible mediator of progressive glomerulosclerosis in this animal model.
肥胖型 Zucker 大鼠会发展出非免疫介导的自发性局灶性肾小球硬化。系膜基质扩张是此类肾小球损伤的一个重要起始标志，而纤连蛋白是系膜细胞外基质的正常组成成分。我们采用基于酶免疫测定的定量方法，评估了肥胖型 Zucker 大鼠及其瘦型同窝仔鼠肾小球内纤连蛋白的含量及其降解情况。在肥胖型 Zucker 大鼠中，肾小球纤连蛋白含量显著高于对照动物。此外，与对照动物相比，肥胖型 Zucker 大鼠肾小球中针对纤连蛋白的蛋白酶活性显著降低。这些数据表明，在肥胖型 Zucker 大鼠中存在纤连蛋白在肾小球内的蓄积，我们认为这至少部分是由于蛋白水解消化减少所致。我们推测，这一结果可能表明在该动物模型中存在一种进行性肾小球硬化的潜在介质。
