Insulin Prevents Depolarization of the Mitochondrial Inner Membrane in Sensory Neurons of Type 1 Diabetic Rats in the Presence of Sustained Hyperglycemia

• DOI: 10.2337/diabetes.52.8.2129
• Publication Date: 2007-03-06T19:04:22Z
• Authors: Tze-Jen Huang; Sally A. Price; Lucy Chilton; Nigel A. Calcutt; David R. Tomlinson; Alex Verkhratsky; Paul Fernyhough
• Keywords: Streptozocin; Diabetic Neuropathy

Mitochondrial dysfunction has been proposed as a mediator of neurodegeneration in diabetes complications. The aim this study was to determine whether deficits insulin-dependent neurotrophic support contributed depolarization the mitochondrial membrane sensory neurons streptozocin (STZ)-induced diabetic rats. Whole cell fluorescent video imaging using rhodamine 123 (R123) used monitor inner potential (Δψm). Treatment cultured dorsal root ganglia (DRG) from normal adult rats for up 1 day with 50 mmol/l glucose had no effect; however, 1.0 nmol/l insulin increased Δψm by 100% (P < 0.05). To role vivo, STZ-induced animals were treated background and DRG analyzed. Insulin therapy effect on raised glycated hemoglobin or sciatic nerve polyol levels, confirming that hyperglycemia unaffected. However, treatment significantly normalized diabetes-induced motor conduction velocity In acutely isolated insulin-treated STZ animals, diabetes-related corrected results demonstrate loss may contribute neuropathy.