Malone J I, Lowitt S, Korthals J K, Salem A, Miranda C
Department of Pediatrics, University of South Florida, Tampa, USA.
Diabetes. 1996 Feb;45(2):209-15. doi: 10.2337/diab.45.2.209.
The nerve conduction velocity (NCV) of nondiabetic male Wistar rats continues to increase until approximately 26 weeks of age. Rats made hyperglycemic at 6 weeks of age manifest reduced NCV by 10 weeks of age and show morphological differences in the sciatic tibial nerve after 5 months of hyperglycemia when compared with age-matched controls. Fiber diameter, myelin width, and the number of large myelinated fibers were decreased in the tibial nerves of the hyperglycemic animals. Rats made hyperglycemic at 26 weeks of age had elevated glycosylated hemoglobin and sciatic nerve sorbitol levels but maintained normal NCVs and had little change in morphology after 7 months of hyperglycemia. Thus, animals with maturing peripheral nerve structure and function exposed to chronic hyperglycemia manifest greater pathological alterations than those that occur when more matured nerves are exposed to similarly elevated glucose concentrations for an even greater duration. We suggest that immature animal models commonly used to study diabetic peripheral neuropathy may not be appropriate for understanding a process that commonly develops in humans who become hyperglycemic after maturation of the peripheral nerves.
非糖尿病雄性Wistar大鼠的神经传导速度（NCV）在约26周龄前持续增加。6周龄时血糖升高的大鼠在10周龄时NCV降低，与年龄匹配的对照组相比，高血糖5个月后坐骨神经胫神经出现形态学差异。高血糖动物的胫神经纤维直径、髓鞘宽度和大的有髓纤维数量减少。26周龄时血糖升高的大鼠糖化血红蛋白和坐骨神经山梨醇水平升高，但NCV保持正常，高血糖7个月后形态变化不大。因此，外周神经结构和功能成熟的动物在慢性高血糖状态下比那些更成熟的神经在更长时间内暴露于同样升高的葡萄糖浓度时出现的病理改变更大。我们认为，常用于研究糖尿病周围神经病变的未成熟动物模型可能不适用于理解在周围神经成熟后血糖升高的人类中常见的发病过程。
