caa a22 4500 475771087 CHVBK 20180406123617.0 cr unu---uuuuu 170329e20000601xx s 000 0 eng 10.1007/s001250051376 doi (NATIONALLICENCE)springer-10.1007/s001250051376 A comparison of diabetic polyneuropathy in Type II diabetic BBZDR/Wor rats and in Type I diabetic BB/Wor rats [Elektronische Daten] [A.A.F. Sima, W. Zhang, G. Xu, K. Sugimoto, D. Guberski, M. A. Yorek] 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.¶Methods. 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.¶Results. 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. [Diabetologia (2000) 43: 786-793] Springer-Verlag Berlin Heidelberg, 2000 Keywords Neuropathy, Type I and Type II diabetes, electrophysiology, structural changes nationallicence Sima A.A.F. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut Zhang W. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut Xu G. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut Sugimoto K. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut Guberski D. Biomedical Research Models Inc., Worcester, Massachusetts, USA, US aut Yorek M. A. Department of Medicine, University of Iowa, Iowa City, Iowa, USA, US aut https://doi.org/10.1007/s001250051376 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s001250051376 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Sima A.A.F. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut NATIONALLICENCE 700 1- Zhang W. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut NATIONALLICENCE 700 1- Xu G. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut NATIONALLICENCE 700 1- Sugimoto K. Departments of Pathology and Neurology, Wayne State University, Detroit, Michigan, USA, US aut NATIONALLICENCE 700 1- Guberski D. Biomedical Research Models Inc., Worcester, Massachusetts, USA, US aut NATIONALLICENCE 700 1- Yorek M. A. Department of Medicine, University of Iowa, Iowa City, Iowa, USA, US aut Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer