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链脲佐菌素诱导的大鼠糖尿病肾小管功能障碍的可逆性

Reversibility of renal tubular dysfunction in streptozotocin-induced diabetes in the rat.

作者信息

Chouinard S, Viau C

机构信息

Département de médecine du travail et hygiène du milieu, Université de Montréal, Québec, Canada.

出版信息

Can J Physiol Pharmacol. 1992 Jul;70(7):977-82. doi: 10.1139/y92-134.

DOI:10.1139/y92-134
PMID:1451036
Abstract

Enzymuria and specific proteinuria were examined over a period of 19 days in 4 groups of 5 rats: a control group, a nondiabetic polyuric group, a group of streptozotocin-induced diabetic rats treated with insulin as of the 10th day after the injection of the drug, and a similar group of untreated diabetic rats. Increased urinary excretion of beta-N-acetyl-D-glucosaminidase, lactate dehydrogenase, and alanine aminopeptidase was observed shortly after the induction of diabetes. It was partly or totally reversible following insulin treatment. Nondiabetic polyuria had a slight effect on the excretion of alanine aminopeptidase only. The urinary excretion of beta 2-microglobulin also rapidly increased after the onset of diabetes to a level approximately 50 times the control values. This effect was largely reversible with insulin treatment and was absent in the nondiabetic polyuric group. A small but significant 3-fold increase in albumin excretion was also noted but was not affected by insulin treatment. We conclude that streptozotocin-induced diabetes causes an early tubular dysfunction that is unrelated to polyuria and is reversible upon insulin treatment. This tubular dysfunction is best revealed by the urinary excretion of the low molecular weight protein beta 2-microglobulin. Our results suggest that it would be of interest to further examine the usefulness of sensitive markers of tubular dysfunction, especially low molecular weight proteinuria, in the detection of early stages of diabetic nephropathy.

摘要

在19天的时间里,对4组每组5只大鼠进行了酶尿和特异性蛋白尿检测:一组为对照组,一组为非糖尿病多尿组,一组为注射链脲佐菌素诱导的糖尿病大鼠,自注射药物后第10天起用胰岛素治疗,另一组为未治疗的糖尿病大鼠。糖尿病诱导后不久,观察到β-N-乙酰-D-氨基葡萄糖苷酶、乳酸脱氢酶和丙氨酸氨基肽酶的尿排泄增加。胰岛素治疗后,这种增加部分或完全可逆。非糖尿病性多尿仅对丙氨酸氨基肽酶的排泄有轻微影响。糖尿病发病后,β2-微球蛋白的尿排泄也迅速增加,达到对照值的约50倍。胰岛素治疗后,这种影响在很大程度上是可逆的,且在非糖尿病多尿组中不存在。白蛋白排泄也有小幅但显著的3倍增加,但不受胰岛素治疗影响。我们得出结论,链脲佐菌素诱导的糖尿病会导致早期肾小管功能障碍,这与多尿无关,且胰岛素治疗后可逆。这种肾小管功能障碍通过低分子量蛋白β2-微球蛋白的尿排泄最能体现。我们的结果表明,进一步研究肾小管功能障碍敏感标志物,尤其是低分子量蛋白尿,在糖尿病肾病早期检测中的有用性将是有意义的。

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Reversibility of renal tubular dysfunction in streptozotocin-induced diabetes in the rat.链脲佐菌素诱导的大鼠糖尿病肾小管功能障碍的可逆性
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