The worldwide prevalence of obesity has reached pandemic proportions, and with it have come other associated metabolic diseases, such as insulin resistance and type 2 diabetes (T2D). Intensive research has identified the frequent coexistence of obesity with a state of inflammation in metabolic tissues such as adipose tissue and liver [1]. Multiple inflammatory and stress responses are evoked in these metabolic tissues, leading to chronic, low grade, local inflammation that plays a central role in the disruption of systemic metabolic homeostasis during the pathogenesis of obesity. This atypical state engages immune response pathways, including recruitment of immune cells into metabolic tissues, activation of IB kinase (IKK) and c-Jun N-terminal kinase (JNK) pathways, and elevated production of an array of immune mediators that impact nutrient metabolism and insulin action [1]. However, the molecular basis for the induction of metabolic inflammation and the vast network of pathological responses remains to be elucidated.