Inflammation and Type 2 Diabetes

This chapter discusses the current insights into how inflammation, particularly obesity-associated low-grade inflammation, may contribute to development of insulin resistance and β-cell failure, and hence comprise a major culprit for the development of type 2 diabetes. For development of type 2 diabetes, at least two major events are necessary. First, the development of insulin resistance, and second the development of β-cell decay. Cardiovascular disease is a major long-term complication of insulin resistance and diabetes. Macrovascular disease is perceived to be a major consequence of obesity-induced inflammation, insulin resistance, and type 2 diabetes. There are several potential targets for control of inflammation and prevention of insulin resistance and type 2 diabetes. The chapter further discusses a selection of these potential targets for intervention, that is, PPAR-γ, the inflammasome, the gut microbiome, the complement system, dicarbonyl compounds/advanced glycation endproducts (AGEs), and lifestyle.