Lipids and inflammatory mediators: integration of metabolic and immune responses in adipocytes and macrophages through shared mechanisms. Under normal conditions, adipocytes store lipids and regulate metabolic homeostasis, and macrophages function in the inflammatory response, although each cell type has the capacity to perform both functions. In obesity, adipose tissue becomes inflamed, both via infiltration of adipose tissue by macrophages and as a result of adipocytes themselves becoming producers of inflammatory cytokines. Inflammation of adipose tissue is a crucial step in the development of peripheral insulin resistance. In addition, in proatherosclerotic conditions such as obesity and dyslipidemia, macrophages accumulate lipid to become foam cells. Adipocytes and macrophages share common features such as expression of cytokines, FABPs, nuclear hormone receptors, and many other factors. As evidenced by genetic loss-of-function models, adipocyte/macrophage FABPs modulate both lipid accumulation in adipocytes and cholesterol accumulation in macrophages, as well as the development of insulin resistance and atherosclerosis. PPARγ and LXR pathways oppose inflammation and promote cholesterol efflux from macrophages and lipid storage in adipocytes.