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.
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.
Authors: Chikodi N Anigbogu; Richard O Speakman; Dennis L Silcox; Laura V Brown; David R Brown; Ming C Gong; Abhijit R Patwardhan; L Raymond Reynolds; Dennis G Karounos; Don E Burgess; Bobby R Baldridge; David C Randall Journal: Auton Neurosci Date: 2012-07-17 Impact factor: 3.145
Authors: Amal Jamil Fatani; Salim Salih Al-Rejaie; Hatem Mustafa Abuohashish; Abdullah Al-Assaf; Mihir Yogeshkumar Parmar; Mohammad Shamsul Ola; Mohammed Mahboobuddin Ahmed Journal: Exp Ther Med Date: 2015-02-20 Impact factor: 2.447
Authors: G J Biessels; V Bril; N A Calcutt; N E Cameron; M A Cotter; R Dobrowsky; E L Feldman; P Fernyhough; J Jakobsen; R A Malik; A P Mizisin; P J Oates; I G Obrosova; R Pop-Busui; J W Russell; A A Sima; M J Stevens; R E Schmidt; S Tesfaye; A Veves; A I Vinik; D E Wright; S Yagihashi; M A Yorek; D Ziegler; D W Zochodne Journal: J Peripher Nerv Syst Date: 2014-06 Impact factor: 3.494