PT - JOURNAL ARTICLE AU - Tan, M. H. TI - The lipoprotein lipase system: new understandings DP - 1978 Mar 18 TA - Canadian Medical Association Journal PG - 675--680 VI - 118 IP - 6 4099 - http://www.cmaj.ca/content/118/6/675.short 4100 - http://www.cmaj.ca/content/118/6/675.full SO - CMAJ1978 Mar 18; 118 AB - Hypertriglyceridemia, a risk factor for premature atherosclerosis, may result from decreased use of plasma triglycerides by tissues. The removal of triglycerides is mediated by the enzyme lipoprotein lipase (LPL). Heparin releases LPL from tissues and post-heparin plasma lipolytic activity (PHLA) has been extensively used to elucidate the mechanism of hypertriglyceridemia in various diseases. There is evidence to show that postheparin plasma contains enzymes other than LPL. Hence data on total PHLA are difficult to interpret. Availability of assays for the LPL component of PHLA has clarified equivocal findings in certain hypertriglyceridemic states. However, the LPL component is also heterogeneous. The LPL "isoenzymes" from various extrahepatic tissues behave differently under various metabolic conditions. Therefore, to understand properly the LPL system it is necessary to study the specific tissue LPL. Furthermore, the serum activator for LPL is now characterized. Its importance is evidenced by the recent discovery of a hypertriglyceridemic patient deficient in this apoprotein.