Inflammation plays a pivotal role in the pathophysiology of atherosclerosis. Remnant-like lipoprotein particles (RLPs) have been implicated as potentially atherogenic lipoproteins. RLPs can induce a pronounced inflammatory response especially during the postprandial phase. Increasing evidence demonstrates that adipose tissue may be a significant contributor to the increased systemic inflammation through secretion of various proinflammatory adipocytokines. In addition, adipocytes may potentially regulate RLPs metabolism. Therefore, we hypothesized that there might be an interaction between RLPs and adipocytes.