Obesity is one of the main rising causes of health problems in modern society and is correlated to type 2 diabetes mellitus, hypertension, heart disease and atherosclerosis. Bacterial products, endogenous substances such as oxidized LDL (ox-LDL) and heat shock proteins mediate activation of Toll-like receptors and reinforce the view that the innate immune system plays a key role in the genesis of atherosclerosis. In addition, natural killer T (NKT) cells respond to lipids presented via CD1d on APCs, and may also be able to affect atherosclerosis. All the main cell types involved in atherosclerosis such as endothelial cells, macrophages, T cells, smooth muscle cells and platelets express proinflammatory cytokines. In addition, CD4 ligation triggers the expression of adhesion molecules, cytokines and matrix metalloprotinease. IL-6 cytokines travels to the liver where it elicits acute phase response resolving in the release of serum amyloid-A C-reactive protein, fibrogen and plasminogen activator inhibitor-1. Therefore increasing body fat mass is associated with high levels of inflammatory cytokines such as IL-1 and TNF. In this study we revisit the interrelationship between fat and inflammation.
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