Diabetic neuropathies: Components of etiology

David R. Tomlinson, Natalie J. Gardiner

    Research output: Contribution to journalArticlepeer-review


    This review examines the putative role of glucose in the etiology of diabetic neuropathies. Excessive glucose generates several secondary metabolic anomalies - principally oxidative stress (via both the polyol pathway and glucoxidation) and non-enzymic glycation of macromolecules. The latter is also facilitated by glucoxidation. These metabolic deviations trigger cellular responses that are inappropriate to normal function. Principal among these are neurotrophic deficits and phosphorylation of mitogen-activated protein kinases (MAPK). Downstream of these events are aberrant ion channel function and disordered gene expression, leading to changes in cellular phenotype. This leads directly to disordered nerve conduction, a recognised early clinical sign, and indirectly, via as yet undisclosed links, to sensory loss and axonopathy. Recent work also links MAPK activation to the development of neuropathic pain. © 2008 Peripheral Nerve Society.
    Original languageEnglish
    Pages (from-to)112-121
    Number of pages9
    JournalJournal of the Peripheral Nervous System
    Issue number2
    Publication statusPublished - Jun 2008


    • Diabetes
    • MAP kinases
    • Nerve conduction
    • Neuropathy
    • Neurotrophins
    • Oxidative stress


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