Neurology Research Seminar
CME CREDIT AVAILABLE, CLICK HERE.
Peripheral neuropathy (PN) is the most common complication of type 2 diabetes (T2D) and prediabetes. Patients with PN experience a length-dependent loss of sensation in their limbs due to peripheral nerve damage. The severity of PN in T2D and prediabetic patients correlates with dyslipidemia indicating that dietary fatty acids contribute to PN pathogenesis. We examined the impact of dietary saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) on nerve function in a murine model of prediabetes. Interestingly, mice fed an SFA-rich high fat diet (HFD) developed robust PN while mice switched to a MUFA-rich HFD had improved nerve function. In vitro, SFA treatments impaired mitochondrial trafficking and function in cultured sensory neurons while MUFA supplementation prevented mitochondrial dysfunction through the formation of lipid droplets. These data suggest that SFA-induced mitochondrial dysfunction contributes to PN development, and that MUFAs restore nerve function and prevent mitochondrial dysfunction through lipid droplet formation.