Rasch R, Osterby R
Department of Cell Biology, University of Aarhus, Denmark.
J Diabet Complications. 1989 Oct-Dec;3(4):198-201. doi: 10.1016/0891-6632(89)90030-5.
Streptozotocin diabetic rats were divided into two groups. One diabetic group was given an aldose reductase inhibitor (Statil) throughout the study and the other group was left untreated. An additional group of nondiabetic rats was included in the study. After 7 months, the kidneys were perfusion fixed and blocks of tissue were sampled systematically and uniformly throughout the kidney cortex. Plastic embedded blocks were sectioned and used to determine the volume fraction of tubular glycogen by light microscopy. No difference was found between the two diabetic groups in glycogen deposits in the cortical thick ascending limb of Henle's loop, expressed as volume fraction per cortex. Tubules from control animals contained no visible glycogen, as opposed to a content of about 1% in both diabetic groups. We concluded that an aldose reductase inhibitor does not aggravate this tubular lesion (i.e., the Armanni-Ebstein lesion) in rats with experimental diabetes.
将链脲佐菌素诱导的糖尿病大鼠分为两组。一组糖尿病大鼠在整个研究过程中给予醛糖还原酶抑制剂（Statil），另一组不进行治疗。另外一组非糖尿病大鼠也纳入研究。7个月后，对肾脏进行灌注固定，并在整个肾皮质系统且均匀地采集组织块。将塑料包埋的组织块切片，通过光学显微镜确定肾小管糖原的体积分数。以每皮质的体积分数表示，在亨利袢皮质厚升支的糖原沉积方面，两个糖尿病组之间未发现差异。与两个糖尿病组约1%的含量相反，对照动物的肾小管中未发现可见的糖原。我们得出结论，醛糖还原酶抑制剂不会加重实验性糖尿病大鼠的这种肾小管病变（即阿曼尼-埃布斯坦病变）。
