DBM小鼠糖尿病性肾小球硬化。定量形态学、免疫荧光和电镜的相关研究]。

Annales d'anatomie pathologique Pub Date : 1980-01-01
G Chomette, J Sterne, M Auriol, P Tranbaloc, J L Junien
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引用次数: 0

摘要

采用遗传性糖尿病(DBM小鼠)实验模型,比较了光镜和电子显微镜所获得的定量数据(肾小球和系膜表面积的测量,基膜厚度及其不规则性的评估),并用于证实31只糖尿病动物肾实质中肾小球硬化的实际存在。此外,这些动物的免疫荧光研究表明,肾小球和肾小管基膜中存在血清蛋白(特别是免疫球蛋白和白蛋白)。由于血管渗透性增加,这些物质穿过血管。在这个区域,膜异常不是高血糖的结果。在该组中,通过糖调节治疗部分降低高血糖的一批动物显示出相同的肾小球变化。除其他因素外,高胰岛素血症在这些动物中持续存在的可能作用,无论其血糖水平如何,都值得考虑。
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[Diabetic glomerulosclerosis in the DBM mouse. Correlated study of quantitative morphology, immunofluorescence and electronic microscopy].

Using an experimental model of genetic diabetes (DBM mouse) a comparison was made of the results of quantitative data obtained by light and electron microscopy (measurement of glomerular and mesangial surface areas, assessment of the thickness of the basal membrane and its irregularities) and was used to demonstrate the actual presence of glomerulosclerosis in the renal parenchyma of 31 diabetic animals. In addition, immunofluorescent investigations in these same animals demonstrated the presence of serum proteins (in particular immunoglobulins and albumin) in the glomerulus and the tubular basal membrane. These substances transude through the vessels as a result of increased vascular permeability. In this area, membrane abnormalities are not a consequence of hyperglycaemia. In the group, one batch of animals in which hyperglycaemia was partially reduced by glycoregulatory therapy showed the same glomerular changes. Amongst other factors, the possible role of hyperinsulinaemia constantly present in these animals, regardless of their blood glucose level, is worthy of considération.

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