• Petra Baum, Joanna Kosacka, Irina Estrela-Lopis, Katrin Woidt, Heike Serke, Sabine Paeschke, Maximilian Stockinger, Nora Klöting, Matthias Blüher, Marco Dorn, Joseph Classen, Joachim Thiery, Ingo Bechmann, Klaus V Toyka, and Marcin Nowicki.
• Department of Neurology, University Hospital Leipzig, Liebigstr. 20, D-04103 Leipzig, Germany.
• Metab. Clin. Exp. 2016 Apr 1; 65 (4): 391-405.

BackgroundIron is an essential but potentially toxic metal in mammals. Here we investigated a pathogenic role of exogenous iron in peripheral diabetic neuropathy (PDN) in an animal model for type 1 diabetes.MethodsDiabetes was induced by a single injection of streptozotocin (STZ) in 4-month-old Sprague-Dawley rats. STZ-diabetic rats and non-diabetic rats were fed with high, standard, or low iron diet. After three months of feeding, animals were tested.ResultsSTZ-rats on standard iron diet showed overt diabetes, slowed motor nerve conduction, marked degeneration of distal intraepidermal nerve fibers, mild intraneural infiltration with macrophages and T-cells in the sciatic nerve, and increased iron levels in serum and dorsal root ganglion (DRG) neurons. While motor fibers were afflicted in all STZ-groups, only a low iron-diet led also to reduced sensory conduction velocities in the sciatic nerve. In addition, only STZ-rats on a low iron diet showed damaged mitochondria in numerous DRG neurons, a more profound intraepidermal nerve fiber degeneration indicating small fiber neuropathy, and even more inflammatory cells in sciatic nerves than seen in any other experimental group.ConclusionsThese results indicate that dietary iron-deficiency rather than iron overload, and mild inflammation may both promote neuropathy in STZ-induced experimental PDN.Copyright © 2016 Elsevier Inc. All rights reserved.

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