Prolonged nutrient surplus causes macrophages to accumulate in the liver and intramuscular visceral fat, triggering synthesis of proinflammatory mediators such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), macrophage chemoattractant protein-1 (MCP-1), matrix metalloproteinases (MMPs), and fatty acid binding protein [1] that contribute to the development of cardiovascular diseases and metabolic syndrome. Here, IL6 is linked to metabolic syndrome.