Cárdenas A, Schadeck C, Bernard A, Lauwerys R
Unit of Industrial Toxicology and Occupational Medicine, Catholic University of Louvain, Brussels, Belgium.
Biochem Med Metab Biol. 1991 Dec;46(3):416-21. doi: 10.1016/0885-4505(91)90089-4.
The role of sialidase in the depletion of glomerular sialic acid induced by diabetes has been investigated in uninephrectomized rats. Four months after streptozotocin administration, diabetic rats showed an enhanced urinary excretion of albumin and transferrin, which was associated with a decrease of sialic acid concentration in isolated glomeruli. Despite the sialic acid depletion, the glomerular sialidase activity was unchanged. These results indicate that the decreased glomerular sialic acid concentration observed in diabetic nephropathy might be caused by a disturbance of the sialylation of glomerular structures.
在单侧肾切除的大鼠中研究了唾液酸酶在糖尿病诱导的肾小球唾液酸耗竭中的作用。给予链脲佐菌素四个月后,糖尿病大鼠的白蛋白和转铁蛋白尿排泄增加,这与分离的肾小球中唾液酸浓度降低有关。尽管唾液酸耗竭,但肾小球唾液酸酶活性未改变。这些结果表明,糖尿病肾病中观察到的肾小球唾液酸浓度降低可能是由肾小球结构唾液酸化紊乱引起的。