Editorial Apolipoprotein

Apolipoprotein CIII (apoCIII) was first identified morethan 40 years ago as a component of very-low-density lipoprotein (VLDL)1 and shortly thereafter as an inhibitor of lipoprotein lipase.2 More than a decade later, apoCIII was found to inhibit lipoprotein remnant uptake by the liver.3 Its relevance to human lipid metabolism was made clear by its absence, along with apolipoprotein AI, in 2 sisters with essentially no plasma high-density lipoprotein and very low triglyceride levels.4 These individuals had marked increases in the fractional removal of TG from VLDL (increased lipoprotein lipase activity) and increased conversion of VLDL to low-density lipoprotein (LDL) (less remnant re-moval).5 These findings spurred investigations at a molecular level, including demonstrations of hypertriglyceridemia in apoCIII transgenic mice6 and decreased TG levels in apoCIII knockout mice.7 In humans, apoCIII levels are associated wit