Fig. 1.

A simplified model of the role of obesity-related inflammation in disease development. Hypertrophied visceral adipocytes secrete MCP-1, recruiting macrophages that secrete inflammatory cytokines including IL-6 and TNF-α. These enter the systemic circulation and stimulate the production of CRP. These inflammatory molecules contribute to peripheral cellular dysfunction of the endoplasmic reticulum and mitochondria, resulting in a worsening of insulin resistance that is further exacerbated by low levels of adiponectin and high levels of free fatty acids. In the intima of arteries, inflammatory molecules including CRP activate monocytes, contributing to reactive oxygen species and the oxidation of LDL-C, which is then taken up by macrophages to form lipid-laden foam cells. Further injury remodeling and fibroblast migration contribute to a growing atherosclerotic plaque. CRP, C-reactive protein; IL-6, interleukin-6; LCL-C, low-density lipoprotein cholesterol; MCP-1, monocyte chemoattractant protein-1; TNF-α, tumor necrosis factor-α.