Asplund-Carlson A, Hamsten A, Wiman B, Carlson L A
King Gustaf V Research Institute, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Diabetologia. 1993 Sep;36(9):817-25. doi: 10.1007/BF00400356.
Impaired fibrinolytic function secondary to elevated plasma plasminogen activator inhibitor-1 activity, hypertriglyceridaemia and hyperinsulinaemia are frequent findings in patients with coronary heart disease. It has been debated whether VLDL or insulin is the major regulator of plasma plasminogen activator inhibitor-1 activity. This study examines the relationships between plasma plasminogen activator inhibitor-1 activity and VLDL triglyceride concentration, fasting and post-oral glucose load insulin levels and insulin sensitivity, as estimated by the minimal model method. Subjects studied were randomly selected hypertriglyceridaemic (n = 65) and age-matched normotriglyceridaemic (n = 61) men, aged 40-50 years, recruited in a population survey. Plasma plasminogen activator inhibitor-1 activity was higher in the hypertriglyceridaemic than in the normotriglyceridaemic group (21 +/- 14 vs 10 +/- 8 mU/l; p < 0.01). The hypertriglyceridaemic group had higher serum insulin, basal as well as 2 h after intake of the oral glucose load, and a lower insulin sensitivity index. In univariate analysis, plasma plasminogen activator inhibitor-1 activity correlated positively with VLDL triglycerides in both the hyper- and normotriglyceridaemic groups (r = 0.43 r = 0.60, respectively) and negatively with the insulin sensitivity index (r = -0.35 r = -0.44, respectively). In multivariate analysis, VLDL triglyceride levels were found to be independently related to plasma plasminogen activator inhibitor-1 activity in both groups, whereas insulin sensitivity/serum insulin levels were not. An unexpected finding was that the serum activity of the enzyme gamma glutamyl transpeptidase appeared to influence the relationships for plasma plasminogen activator inhibitor-1 in the hypertriglyceridaemic group.(ABSTRACT TRUNCATED AT 250 WORDS)
冠心病患者常出现因血浆纤溶酶原激活物抑制剂-1活性升高、高甘油三酯血症和高胰岛素血症继发的纤溶功能受损。关于极低密度脂蛋白（VLDL）或胰岛素是否为血浆纤溶酶原激活物抑制剂-1活性的主要调节因子一直存在争议。本研究采用最小模型法，探讨血浆纤溶酶原激活物抑制剂-1活性与VLDL甘油三酯浓度、空腹及口服葡萄糖负荷后胰岛素水平以及胰岛素敏感性之间的关系。研究对象为在一项人群调查中随机选取的40 - 50岁高甘油三酯血症男性（n = 65）和年龄匹配的正常甘油三酯血症男性（n = 61）。高甘油三酯血症组的血浆纤溶酶原激活物抑制剂-1活性高于正常甘油三酯血症组（21±14 vs 10±8 mU/l；p < 0.01）。高甘油三酯血症组血清胰岛素水平在基础状态及口服葡萄糖负荷后2小时均较高，且胰岛素敏感性指数较低。单因素分析中，高甘油三酯血症组和正常甘油三酯血症组的血浆纤溶酶原激活物抑制剂-1活性均与VLDL甘油三酯呈正相关（分别为r = 0.43和r = 0.60），与胰岛素敏感性指数呈负相关（分别为r = - 在多因素分析中，发现两组中VLDL甘油三酯水平均与血浆纤溶酶原激活物抑制剂-1活性独立相关，而胰岛素敏感性/血清胰岛素水平则不然。一个意外发现是，γ-谷氨酰转肽酶的血清活性似乎影响高甘油三酯血症组中血浆纤溶酶原激活物抑制剂-1的关系。（摘要截断于250字） 0.35和r = - 0.44）。
