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Back: Reducing Oxidative Stress
Abstract
PURPOSE: Oxidative stress is the major mechanism thought to cause the microvascular and macrovascular complications commonly associated with type 2 diabetes.  This paper will examine the evidence linking oxidative stress with long-term complications and discuss methods for minimizing its effect.

METHODS: a PubMed search of the literature was performed to identify the studies discussed in this review.

RESULTS: Although chronic hyperglycemia can be effectively monitored and targeted using A1C concentrations, postprandial glucose levels are also very important.  Postprandial glucose excursions are exhibited by almost all patients with type 2 diabetes and are independent risk factors for cardiovascular morbidity and mortality.  Furthermore, glucose fluctuations during the postprandial period elicit more oxidative stress than chronic sustained hyperglycemia and can lead to endothelial dysfunction, vascular inflammation, and microvascular complications.  In turn, endothelial dysfunction has been implicated in the development of vascular pathologies such as atherosclerosis. Pharmacological interventions, such as rapid-acting insulin analogs that target postprandial glucose excursions, reduce oxidative stress, reduce vascular inflammation, and improve endothelial dysfunction. 

CONCLUSIONS: Given the important role of oxidative stress in the development of complications associated with type 2 diabetes, it is important that physicians consider methods to reduce oxidative stress that may occur during both acute (postprandial) and chronic hyperglycemia.  One critical aspect of this will be to reduce postprandial glucose levels to <180 mg/dL while lowering fasting glucose levels to <110 mg/dL.  By coaching patients to reach these goals, physicians and other healthcare colleagues will minimize the risk of long-term complications associated with type 2 diabetes. Read More