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Abstract
Sensory neurons in diabetes may be primarily targeted by diabetes and their involvement may account for prominent sensory loss and pain in diabetic patients. Previous studies demonstrating evidence of excessive polyol flux, microangiopathy, and oxidative stress involving sensory axons and ganglia have been joined by more recent work demonstrating altered neuron phenotype, mitochondrial dysfunction, ion channel alterations, and abnormal growth factor signaling. As such, an interesting and unique panoply of molecular changes in primary sensory neurons has been identified in diabetic models. Insulin deficiency and subsequent changes in second messenger signaling may also play an important role in how sensory neurons respond to diabetes. Applying approaches to support sensory neurons in diabetes may be an important therapeutic direction in diabetic patients.