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Although the concept of inflammatory obesity remains to be widely accepted, a plethora of antibiotics, anti-inflammatory agents, mitochondrial uncouplers, and other structurally distinct compounds with unknown mechanisms have been demonstrated to exert functionally identical effects on weight reduction. Here we summarize a universal mechanism in which weight loss is modulated by mitochondrial biogenesis, which is correlated with conversion from the mitochondria-insufficient white adipose tissue to the mitochondria-abundant brown adipose tissue. This mechanistic description of inflammatory obesity may prove useful in the future for guiding pathology-based drug discovery for weight reduction.