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Metabolism. 2016 Apr;65(4):391-405. doi: 10.1016/j.metabol.2015.11.002. Epub 2015 Nov 6.

The role of nerve inflammation and exogenous iron load in experimental peripheral diabetic neuropathy (PDN).

Author information

1
Department of Neurology, University Hospital Leipzig, Liebigstr. 20, D-04103 Leipzig, Germany.
2
Department of Medicine, University of Leipzig, Liebigstr. 21, D-04103 Leipzig, Germany.
3
Institute of Medical Physics and Biophysics, University of Leipzig, Härtelstr. 16-18, D-04107 Leipzig, Germany.
4
Institute of Anatomy, University of Leipzig, Liebigstr. 13, D-04103 Leipzig, Germany.
5
Department of Medicine, University of Leipzig, Liebigstr. 21, D-04103 Leipzig, Germany; Integrated Research and Treatment Center (IFB) Adiposity Disease, Liebigstr. 21, D-04103 Leipzig, Germany.
6
Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics (ILM), University of Leipzig, Liebigstr. 27, D-04103 Leipzig, Germany.
7
Department of Neurology, University of Würzburg, Josef-Schneider-Str. 11, D-97080 Würzburg, Germany.
8
Institute of Anatomy, University of Leipzig, Liebigstr. 13, D-04103 Leipzig, Germany. Electronic address: Marcin.Nowicki@medizin.uni-leipzig.de.

Abstract

BACKGROUND:

Iron 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.

METHODS:

Diabetes 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.

RESULTS:

STZ-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.

CONCLUSIONS:

These results indicate that dietary iron-deficiency rather than iron overload, and mild inflammation may both promote neuropathy in STZ-induced experimental PDN.

KEYWORDS:

Iron; Nerve inflammation; Peripheral diabetic neuropathy; STZ-rats; Type 1 diabetes mellitus

PMID:
26975531
DOI:
10.1016/j.metabol.2015.11.002
[Indexed for MEDLINE]

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