Cucuianu M, Brudaşca Ioana
Medical Clinic I, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Rom J Intern Med. 2008;46(2):99-104.
More than 40 years ago, our laboratory reported that post-heparin lipolytic activity was decreased in patients with severe atherosclerotic disease, while values recorded in obese and hyperlipidemic subjects without clinically detectable atherosclerotic lesions did not significantly differ from normal weight normolipidemic controls. Because in 1967 data on pathophysiology of lipolytic enzymes were rather scarce, and mainly because our information facilities were limited in those years, we had difficulties in interpreting these results, and the study was to some extent awkwardly approached, as the investigated subjects were not considered according to their gender, body fat patterning and type of hyperlipoproteinemia, and the lipolytic activities of lipoprotein lipase and hepatic lipase had not been selectively assessed. Reviewing recent data in the literature it was noted that pre-heparin lipoprotein lipase mass assessed by ELISA was indeed significantly lower in insulin resistant coronary patients than in patients with no lesions, and correlated negatively with the severity of atherosclerotic lesions. Noteworthy hypoadiponectinemia, a hallmark of insulin resistance, was associated with decreased lipoprotein lipase and increased hepatic lipase activities. Clustering of increased plasma VLDL-triglyceride, cholesteryl-ester transfer protein and hepatic lipase would remodel HDL and LDL particles, generating an atherogenic lipoprotein profile. In opposition to atherogenic dyslipidemia related to an enhanced hepatic secretion of VLDL, cases with important hypertriglyceridemia subsequent to deficient lipolytic clearance are at a rather low risk for coronary artery disease. It may therefore be suggested that the decreased lipoprotein lipase noted in atherosclerotic patients is not a major pathogenic link, being rather related to the inflammatory component of the disease, its expression being reduced by proinflammatory cytokines.
40多年前，我们的实验室报告称，严重动脉粥样硬化疾病患者的肝素后脂解活性降低，而在没有临床可检测到动脉粥样硬化病变的肥胖和高脂血症受试者中记录的值与正常体重血脂正常的对照组相比没有显著差异。由于1967年关于脂解酶病理生理学的数据相当稀少，主要是因为那些年我们的信息设施有限，我们在解释这些结果时遇到了困难，而且这项研究在某种程度上处理得很笨拙，因为没有根据受试者的性别、体脂分布和高脂蛋白血症类型来考虑研究对象，也没有选择性地评估脂蛋白脂肪酶和肝脂肪酶的脂解活性。回顾文献中的最新数据发现，通过酶联免疫吸附测定法评估的胰岛素抵抗性冠心病患者的肝素前脂蛋白脂肪酶质量确实显著低于无病变患者，并且与动脉粥样硬化病变的严重程度呈负相关。值得注意的是，胰岛素抵抗的一个标志——低脂联素血症与脂蛋白脂肪酶降低和肝脂肪酶活性增加有关。血浆极低密度脂蛋白甘油三酯、胆固醇酯转移蛋白和肝脂肪酶增加的聚集会重塑高密度脂蛋白和低密度脂蛋白颗粒，产生致动脉粥样硬化的脂蛋白谱。与因极低密度脂蛋白肝脏分泌增加相关的致动脉粥样硬化血脂异常相反，脂解清除不足导致严重高甘油三酯血症的患者患冠状动脉疾病的风险相当低。因此，可能有人认为，动脉粥样硬化患者中脂蛋白脂肪酶降低不是一个主要的致病环节，而更可能与疾病的炎症成分有关，其表达会被促炎细胞因子降低。
