Ino-ue M, Yokogawa H, Yamamoto M, Naka H, Kuriyama H
Department of Ophthalmology, School of Medicine, Kobe University, Kobe, Japan.
Exp Eye Res. 1998 Apr;66(4):397-401. doi: 10.1006/exer.1997.0426.
Structural impairments of optic nerve fibers in the streptozotocin-induced diabetic rat were investigated using morphometric analysis. The effect of aldose reductase inhibitor (ARI) on abnormalities in myelinated nerve fibers was also evaluated. Three months after the induction of diabetes, loss of body weight and significantly elevated levels of serum glucose were observed. Light microscopic examination revealed that the mean size of the optic nerve in the diabetic rat remained unchanged. Electron microscopic morphometry showed the significantly smaller cross-sectional size of axons and myelin but no change of myelinated fiber number. Reductions of myelinated fiber size was especially remarkable in the larger fibers. ARI treatment improved structural abnormalities without any changes in body weight and blood glucose level. Reduction of axon size and myelin/axon ratio was completely inhibited by ARI treatment. These findings suggest that structural impairment may contribute to the abnormalities of psychophysical and electrophysiological measurements detected in diabetes. Moreover, ARI treatment, which can improve the polyol metabolism, may have a beneficial effect on optic nerve impairment in diabetes.
利用形态计量学分析研究链脲佐菌素诱导的糖尿病大鼠视神经纤维的结构损伤。还评估了醛糖还原酶抑制剂（ARI）对有髓神经纤维异常的影响。糖尿病诱导三个月后，观察到体重减轻和血清葡萄糖水平显著升高。光学显微镜检查显示糖尿病大鼠视神经的平均大小保持不变。电子显微镜形态计量学显示轴突和髓鞘的横截面积显著变小，但有髓纤维数量没有变化。有髓纤维大小的减小在较大纤维中尤为明显。ARI治疗改善了结构异常，而体重和血糖水平没有任何变化。ARI治疗完全抑制了轴突大小和髓鞘/轴突比率的降低。这些发现表明，结构损伤可能导致糖尿病中检测到的心理物理学和电生理学测量异常。此外，能够改善多元醇代谢的ARI治疗可能对糖尿病性视神经损伤有有益作用。
