Abstract
Type 2 diabetes develops due to the initial development of insulin resistance in various tissues, including skeletal muscle and liver, coupled with a relative failure of pancreatic beta-cells to secrete insulin. While the etiology of insulin resistance is multifactorial, accumulating evidence indicates that one cause of this dysfunction in insulin action is oxidative stress, represented by an imbalance between oxidant production and antioxidant mechanisms. Oxidative stress can develop due to overactivity of the renin-angiotensin system, nutrient excess and mitochondrial dysfunction, dyslipidemia, and endoplasmic reticulum stress. Antioxidant interventions, including alpha-lipoic acid, can ameliorate oxidative stress and improve insulin action in conditions of oxidative stress.
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