Oxidative injury and neuropathy in diabetes and impaired glucose tolerance |
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| Authors: | Russell James W Berent-Spillson Alison Vincent Andrea M Freimann Catherine L Sullivan Kelli A Feldman Eva L |
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| Affiliation: | bDepartment of Neurology, University of Maryland, 22 South Greene Street, Baltimore, MD 21201, USA;cVeterans Affairs Medical Center, Baltimore, MD, USA;dDepartment of Neurology, University of Michigan, USA;eMolecular and Behavioral Neuroscience Institute, University of Michigan, USA;fNovartis Pharmaceuticals, East Hanover, New Jersey, USA |
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| Abstract: | Clinical studies suggest that impaired glucose tolerance (IGT) is associated with the development of neuropathy. The aim of the current study was to determine if neuropathy developed in the female Zucker Diabetic Fatty (ZDF) rat, an animal model of IGT and type 2 diabetes. The ZDF rat develops impaired glucose tolerance (IGT) when fed a control diet, and frank diabetes when fed a high fat diet. Following 10 weeks of hyperglycemia, sensory nerve action potentials (SNAP) and compound motor action potentials (CMAP) were reduced and sensory conduction velocities were slowed (distal > proximal) in the tail and hind limb in ZDF animals with IGT and frank diabetes (p < 0.01). Neuropathy was coupled with evidence of increased reactive oxygen species (ROS) and cellular injury in dorsal root ganglion (DRG) neurons from IGT animals. Our study supports the hypothesis that neuropathy develops in an animal model of IGT and is associated with evidence of oxidative injury in DRG and peripheral nerves. |
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| Keywords: | Neuropathy Diabetes Impaired glucose tolerance Oxidative stress Axons Dorsal root ganglia Schwann cells |
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