Abstract
Oxidative stress plays a pivotal role in the development of diabetes and diabetic complications. Oxidative stress resulting from various etiologies including environmental exposure, lifestyle changes, and systemic inflammation can damage pancreatic β cells, leading to insulin deficiency and type 1 diabetes. It can also induce insulin resistance in peripheral tissues, leading to type 2 diabetes. Metabolic abnormalities associated with diabetes can also cause overproduction of mitochondrial superoxides that in turn generate excessive reactive oxygen or nitrogen species, resulting in multiorgan damage and diabetic complications. In support of this notion, extensive studies using transgenic mouse models overexpressing antioxidant genes and supplementation of exogenous antioxidants in animal models highlight the importance of interfering with oxidative stress pathways in the prevention of diabetes and diabetic complications. In this chapter, we briefly summarize evidence to support the importance of oxidative and/or nitrosative stress pathways in the development of diabetes and diabetic complications.
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