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.

LPL plays a pivotal role in lipids and the metabolism of lipoprotein. Major functions of LPL include the hydrolysis of TG-rich lipoproteins and release of non-esterified fatty acid (NEFA), which are taken up and used for metabolic energy in peripheral tissue such as muscle, or are re-esterified into TG and stored in adipose tissue. The balance between these competing effects could determine whether increased LPL activity will lead to a reduced rate of weight gain or to increased adiposity through increased rates of adipose tissue storage of TG. An imbalance of LPL activity may alter the partitions of plasma TG between muscle and adipose tissue, and thus influence insulin resistance and obesity The top journals are peer reviewed scholarly journals.