Lipoprotein lipase (LPL) catalyzes the rate-limiting step in catabolism of triacylglycerol-rich lipoproteins (TRLs) to make fatty acids and monoacylglycerols available for use in tissue cells. This reaction occurs at ‘binding-lipolysis sites’ at the vascular endothelium and involves a number of factors that together control where and at what rate the triacylglycerols are hydrolyzed. The main factor in development of hypertriglyceridemia is impaired clearance, presumably because of dysfunction of the LPL system. Dysfunction of the LPL system increases the risk for metabolic disease connected to obesity and diabetes[.