Inflammation is a coordinated response to harmful stimuli, with the goal of returning the system back to a normal baseline. The inflammatory response triggered by obesity involves many components of the classical inflammatory response to pathogens and includes systemic increases in circulating inflammatory cytokines and acute phase proteins (e.g., C-reactive protein), recruitment of leukocytes to inflamed tissues, activation of tissue leukocytes, and generation of reparative tissue responses (e.g., fibrosis; ref. 2). However, the nature of obesity-induced metainflammation is unique compared with other inflammatory paradigms (e.g., infection, autoimmune disease) in several key aspects. The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time. Childhood obesity may place individuals at risk for lifelong metainflammation, since inflammatory markers are elevated in obese children as young as 3 years old (3). Superimposed on this chronic inflammation are recurrent acute episodes of nutrition-related immune activation induced by nutrient availability (fasting or high-fat meals) (4–6).