Role of Inflammasomes in Obesity

The adaptive expansion of adipose tissue during energy excess involves significant tissue remodeling and angiogenesis that requires controlled local proinflammatory responses. However, sustained adipose tissue inflammation associated with chronic obesity adversely impacts adipose tissue function and is a major instigator of metabolic diseases such as type 2 diabetes. Despite the absence of overt infection in obesity, the adipose tissue of overweight and obese patients is infiltrated with a substantially high frequency of cells of hematopoietic lineage. A large body of evidence suggests that activated innate immune cell subsets chiefly contribute to the persistent state of inflammation and maybe a common mechanism of several obesity-associated chronic diseases. It has been suggested that lipid fluxes in the adipose tissue and the presence of damage-associated molecular patterns serve as a potential trigger for macrophage infiltration and activation. Emerging evidence shows that inflammasomes, the multiprotein platforms that control the activation and secretion of IL-1 beta and IL-18 in adipose tissue, impact the adipocyte function and T cell activation. This chapter discusses the mechanisms that regulate inflammasome activation in obesity and dietary and pharmacological approaches to control immune-metabolic interactions that link sustained adiposity to chronic diseases. Copyright (C) 2013 S. Karger AG, Basel