ice expressing this transgene, denoted EC-hLpL and L for low and H for high expression, had decreased plasma TG levels compared with wild-type mice (WT): 106±31 in WT, 37±17 (line H), and 63±31 mg/dL (line L) because of a reduction in VLDL TG; plasma cholesterol and HDL levels were unaltered. Crossing a high expressing EC-hLpL transgene onto the LpL knockout background allowed for survival of the pups; TG in these mice was approximately equal to that of heterozygous LpL knockout mice.

Lipoprotein lipase has long been known to hydrolyse triglycerides from triglycerides-rich lipoproteins. More recently, it has been shown to promote the binding of lipoproteins to various lipoprotein receptors. Evidence is also presented regarding the possible atherogenic role of lipoprotein lipase. In theory, lipoprotein lipase deficiency should help to clarify this question. However, the rarity of this condition means that it has not been possible to conduct epidemiological studies. An alternative approach is to investigate the correlation of lipoprotein lipase with onset of cardiovascular disease in prospective studies in large population-based cohorts. Complementary with this approach, animal models have been used to explore the atherogenicity of lipoprotein lipase expressed by macrophages.