Sima A A, Zhang W, Xu G, Sugimoto K, Guberski D, Yorek M A
Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA.
Diabetologia. 2000 Jun;43(6):786-93. doi: 10.1007/s001250051376.
AIMS/HYPOTHESIS: To examine the functional, metabolic and structural abnormalities in peripheral nerve in the spontaneously Type II (non-insulin-dependent) diabetic BBZDR/Wor rat and compare these data with those in the Type I (insulin-dependent) diabetic BB/Wor rat.
Animals were examined at 6 and 14 months of diabetes. Nerve conduction velocity was measured longitudinally. Nerve polyols were analysed using gas liquid chromatography and Na/K(+)-ATPase activity was measured enzymatically. Light and electron microscopic techniques were used for nerve morphometry.
Diabetic BBZDR/Wor rats showed a slowly progressive nerve conduction defect that reached 17% (p < 0.01) at 14 months. There was a decrease in Na+/K(+)-ATPase of 35% (p < 0.05). Structurally, there were mild myelinated fibre atrophy (p < 0.05), mild or absent changes of the node of Ranvier, but significant (p < 0.001) segmental demyelination and Wallerian degeneration. These findings point to a more severe nerve conduction defect, severe myelinated fibre atrophy and profound nodal changes in Type I spontaneously diabetic BB/Wor rats maintained at the same hyperglycaemic concentrations.
CONCLUSION/INTERPRETATION: We conclude that other factors, beside hyperglycaemia, are involved in the pathogenesis of the more severe Type I diabetic neuropathy which possibly involve insulin and C-peptide deficiencies.
目的/假设：研究自发性II型（非胰岛素依赖型）糖尿病BBZDR/Wor大鼠周围神经的功能、代谢和结构异常，并将这些数据与I型（胰岛素依赖型）糖尿病BB/Wor大鼠的数据进行比较。
在糖尿病6个月和14个月时对动物进行检查。纵向测量神经传导速度。使用气相色谱法分析神经多元醇，并通过酶法测量Na/K(+)-ATP酶活性。采用光镜和电镜技术进行神经形态测量。
糖尿病BBZDR/Wor大鼠表现出缓慢进展的神经传导缺陷，在14个月时达到17%（p < 0.01）。Na+/K(+)-ATP酶减少35%（p < 0.05）。在结构上，有轻度有髓纤维萎缩（p < 0.05），郎飞结轻度改变或无改变，但有明显的（p < 0.001）节段性脱髓鞘和华勒变性。这些发现表明，在相同高血糖浓度下维持的I型自发性糖尿病BB/Wor大鼠存在更严重的神经传导缺陷、严重的有髓纤维萎缩和明显的结改变。
结论/解读：我们得出结论，除高血糖外，其他因素也参与了更严重的I型糖尿病神经病变的发病机制，这可能与胰岛素和C肽缺乏有关。
