[WCN23_Plenary:01]
Eva L. Feldman (United States of America)
Type 2 diabetes (T2D) prevalence has reached epidemic proportions, with a concomitant rise in complications, including diabetic neuropathy (DN). DN causes significant morbidity and lowered quality-of-life, and lacks effective disease-modifying therapies.
DN pathogenesis is complex, but insight into disease pathways and risk factors could suggest rational, mechanism-based therapies. Recent clinical studies and meta-analyses indicate glucose control only modestly improves neuropathy in T2D, and that obesity may contribute to DN risk, independent of glycemia. These clinical observations parallel data from the laboratory showing nerve injury is driven by both hyperglycemia and dyslipidemia, but centered on energy failure. Within long peripheral nerve axons, mitochondria, the energy source, must traffic large distances from the cell body to termini. As trafficking and energy production fail at distal sites, nerve injury ensues in a distal-to-proximal manner, mirroring DPN symptomatology in T2D patients.
The only current disease-modifying therapies consist of lifestyle modifications, specifically diet and exercise. Thus, the global burden of.DN is high, with >50% of persons with T2D developing DN. Of the half billion people with T2D, one-third will develop a foot ulcer, with the highest incidence in persons with DN.
As the T2D epidemic spreads from North America, Europe, and Australia, into Asia and Africa, DN is now a leading cause of worldwide disability secondary to ulcers, amputations, and poor quality-of-life with a considerable, growing economic burden to worldwide healthcare systems. Successful DN management requires education, integrated foot care, and lifestyle modifications, measures desperately needed to address this debilitating global disorder.
15 Oct 2023