Tan M H
Can Med Assoc J. 1978 Mar 18;118(6):675-80.
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.
高甘油三酯血症是早发性动脉粥样硬化的一个危险因素,可能是由于组织对血浆甘油三酯的利用减少所致。甘油三酯的清除是由脂蛋白脂肪酶(LPL)介导的。肝素可从组织中释放LPL,肝素后血浆脂解活性(PHLA)已被广泛用于阐明各种疾病中高甘油三酯血症的机制。有证据表明,肝素后血浆中除了LPL外还含有其他酶。因此,关于总PHLA的数据难以解释。PHLA中LPL成分检测方法的出现澄清了某些高甘油三酯血症状态下的模糊结果。然而,LPL成分也是异质性的。来自各种肝外组织的LPL“同工酶”在不同的代谢条件下表现不同。因此,为了正确理解LPL系统,有必要研究特定组织的LPL。此外,现在已经对LPL的血清激活剂进行了表征。最近发现一名缺乏这种载脂蛋白的高甘油三酯血症患者,这证明了其重要性。