Dorsal Root Ganglia Mitochondrial Biochemical Changes in Non-diabetic and Streptozotocin-Induced Diabetic Mice Fed with a Standard or High-Fat Diet

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...

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Veröffentlicht in:Journal of neurology and neuroscience 2017, Vol.8 (2)
Hauptverfasser: Guilford, B L, Ryals, J M, Lezi, E, Swerdlow, R H, Wright, D E
Format: Artikel
Sprache:eng
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Zusammenfassung: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. 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. Complex III subunit Core-2 and voltage dependent anion channel were increased (by 36% and 28% respectively, p
ISSN:2171-6625
2171-6625
DOI:10.21767/2171-6625.1000180