Abstract
Patients suffering from DN (diabetic neuropathy) suffer from the coexistence of positive (i.e. pain, hypersensitivity, tingling, cramps, cold feet, etc.) and negative (i.e. loss of sensory perception, delayed wound healing, etc.) symptoms. Elevated blood glucose alone cannot explain the development and progression of DN. Recently it has been shown that the endogenous reactive metabolite MG (methylglyoxal), elevated as a consequence of reduced Glo1 (glyoxalase I), can contribute to the gain of function via post-translational modification of neuronal ion channels involved in chemosensing and action potential generation in nociceptive nerve endings. The effects of dicarbonyls on the neuronal compartment provides a unifying mechanism for the development of DN. Targeting the accumulation and effects of MG may therefore provide new, more effective, therapeutic approaches for the treatment of DN.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
