Key result
Glycemic control and various pharmacological therapies can manage symptoms of diabetic autonomic neuropathy, though optimal control of blood sugar and blood pressure remains obligatory to prevent its progression.
This review summarizes the pathogenesis, animal models, and therapeutic approaches for managing diabetic autonomic neuropathy, highlighting oxidative stress as a unifying mechanism.
May guide symptom management in diabetic autonomic neuropathy; leaves open prospective validation of targeted therapies.
Diabetic autonomic neuropathy is a debilitating complication of diabetes which can cause heart disease, gastrointestinal symptoms, genitourinary disorders and metabolic diseases. Hyperglycemia induces glucose flux through the polyol pathway; excess/inappropriate activation of Protein Kinase C (PKC) isoforms; accumulation of Advanced Glycation End products (AGE's) and these pathways are associated with metabolic and/or redox state of the cell. Activation of these metabolic pathways leads to oxidative stress which is a mediator of hyperglycemia induced cell injury and is a unifying theme for all mechanisms of diabetic autonomic neuropathy. Glycemic control can slow the onset of diabetic autonomic neuropathy and may reverse it. Pharmacologic and non-pharmacologic therapies are available to treat various symptoms of diabetic autonomic neuropathy. This review focuses on the pathology, animal models and therapeutic approaches available for the management of diabetic autonomic neuropathy.
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Navpreet Kaur (2014) conducted a review in Diabetic Autonomic Neuropathy. Pharmacological and non-pharmacological therapies was evaluated. Glycemic control and various pharmacological therapies can manage symptoms of diabetic autonomic neuropathy, though optimal control of blood sugar and blood pressure remains obligatory to prevent its progression.
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