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Background: Mitochondrial dysfunction is purported as a contributory mechanism underlying diabetic neuropathy, but a defined role for damaged mitochondria in diabetic nerves remains unclear, particularly in standard diabetes models. Experiments here used a high-fat diet in attempt to exacerbate the severity of diabetes and expedite the time-course in which mitochondrial dysfunction may occur. We hypothesized a high-fat diet in addition to diabetes would increase stress on sensory neurons and worsen mitochondrial dysfunction., Methods: Oxidative phosphorylation proteins and proteins associated with mitochondrial function were quantified in lumbar dorsal root ganglia. Comparisons were made between non-diabetic and streptozotocin-induced (STZ) C57Bl/6 mice fed a standard or high-fat diet for 8 weeks., Results: Complex III subunit Core-2 and voltage dependent anion channel were increased (by 36% and 28% respectively, p<0.05) in diabetic mice compared to nondiabetic mice fed the standard diet. There were no differences among groups in UCP2, PGC-1α, PGC-1β levels or Akt, mTor, or AMPK activation. These data suggest compensatory mitochondrial biogenesis occurs to offset potential mitochondrial dysfunction after 8 weeks of STZ-induced diabetes, but a high-fat diet does not alter these parameters., Conclusion: Our results indicate mitochondrial protein changes early in STZ-induced diabetes. Interestingly, a high-fat diet does not appear to affect mitochondrial proteins in either nondiabetic or STZ- diabetic mice., Competing Interests: Competing Interests None.

Abstract: Recent years have brought increased awareness of and attention to the non-motor aspects of Parkinson''s disease. Non-motor features encompass a surprisingly broad clinical spectrum that includes sensory dysfunction, behavioral abnormalities, autonomic impairment, sleep disturbances, and fatigue. Some of these features, such as impaired olfaction, REM sleep behavior disorder, and constipation, may develop long before the classic motor features of Parkinson''s disease make their appearance, while others emerge in concert with disease progression. The early emergence of some non-motor features presents diagnostic opportunities, while the dopa-unresponsiveness of others poses treatment challenges, especially in the advanced stages of the disease. [Copyright &y& Elsevier]