There is a limited understanding of the mechanisms that cause diabetic neuropathy. This study showed that increased concentrations of methylglyoxal — production of which is enhanced by elevated glucose concentrations — may be involved in metabolic hyperalgesia. After demonstrating that individuals with diabetic neuropathy had high methylglyoxal concentrations, the authors showed that methylglyoxal caused post-translational modifications of the Nav1.8 sodium channel that were associated with increased firing of nociceptive neurons. In mouse models of diabetes, a methylglyoxal scavenger reduced hyperalgesia.
ORIGINAL RESEARCH PAPER
Bierhaus, A. et al. Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy. Nature Med. 18, 926–933 (2012)
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Harrison, C. A mechanism of metabolically driven pain. Nat Rev Drug Discov 11, 518 (2012). https://doi.org/10.1038/nrd3798
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DOI: https://doi.org/10.1038/nrd3798