Dietary excess and obesity cause lipid accumulation in adipocytes, initiating a state of cellular stress and activation of JNK and NF-κB. These inflammatory signaling pathways regulate protein phosphorylation and cellular transcriptional events, thereby leading to increased adipocyte production of proinflammatory cytokines, including TNF-α, IL-6, leptin, and resistin, chemokines such as MCP-1, and other proatherogenic mediators, for example PAI-1. Endothelial adhesion molecules (e.g., ICAM-1 and VCAM-1) and chemoattractant molecules (designated CCX) bind integrins and chemokine receptors (CCR), respectively, on the monocyte surface to recruit them to the adipose tissues. The monocytes that differentiate into macrophages produce many of the same inflammatory cytokines and chemokines as those listed above, and additional ones, to further promote local inflammation and propagate the inflammatory diathesis systemically. pS, phosphoserine.