New developments in diabetic neuropathy.
OBJECTIVE
Diabetic neuropathy is a debilitating consequence of type 1 and 2 diabetes. Hyperglycemia disrupts the normal function of neurons and their supporting glia at multiple levels. The complexity of this complication, combined with difficulties of delivering therapy to sensory, sympathetic and parasympathetic neurons, contributes to the intractability of this serious diabetic complication. This review summarizes recent reviews examining the state of research on and treatment of diabetic neuropathy and highlights areas of clinical and basic research that may yield new diagnostic and treatment options.


RESULTS
Recent reviews summarize the effects of hyperglycemia on the peripheral nervous system as well as diagnosis and treatment of patients with diabetic neuropathy. Advances in the analysis of intraepidermal fiber densities could shorten the time course of clinical trials and extend data analyses to include sympathetic as well as sensory information. Unchecked glucose-mediated oxidative stress and advanced glycation endproduct signaling through receptors for advanced glycation endproducts are implicated in diabetic neuropathy and may serve as new therapeutic targets.


CONCLUSIONS
The best efforts of countless investigators have yet to find effective treatments either to stop the progression of axonal degeneration and cell death or regrow damaged axons. Basic research into the prevention of oxidative stress caused by excess glucose as well as the prevention of advanced glycation endproduct/receptor for advanced glycation endproduct signaling may offer new therapeutic targets. The use of skin biopsies may aid in early detection of both sensory and autonomic neuropathy, and perhaps in the case of patients with type 2 diabetes, diagnose neuropathy prior to the onset of symptoms.
Sullivan
Kelli A
KA
Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109, USA.
Feldman
Eva L
EL
D000818:Animals; D001706:Biopsy / Q000379:methods; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D018009:Receptors, Glycine / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D012867:Skin / Q000473:pathology
D018009:Receptors, Glycine