Silveira A, Karpe F, Blombäck M, Steiner G, Walldius G, Hamsten A
Department of Clinical Chemistry, King Gustaf V Research Institute, Karolinska Hospital, Stockholm, Sweden.
Arterioscler Thromb. 1994 Jan;14(1):60-9. doi: 10.1161/01.atv.14.1.60.
Dietary studies have established a connection between plasma lipoproteins and coagulation factor VII. The present study was undertaken to specifically examine whether factor VII is activated during alimentary lipemia and to investigate the relations of factor VII mass and activity state with fasting and postprandial lipoproteins and free fatty acids (FFAs). Factor VII levels were therefore determined in plasma samples taken before and after intake of a standardized, oral fat load of a mixed-meal type in 33 men (mean age +/- SD, 48.8 +/- 3.2 years) with a previous myocardial infarction at a young age and 10 healthy, age-matched control subjects. A panel of methods for factor VII determination was used to ensure that changes in all potentially existing forms of the factor during alimentary lipemia would be included. Substantial activation of factor VII was found to occur during alimentary lipemia, whereas the number of factor VII molecules remained constant or even appeared to decrease after the test meal. Activation of factor VII was more pronounced in control subjects than patients, and the proportion of activated factor VII molecules was higher in control subjects. Interestingly, factor VII activation, which correlated quantitatively with the degree of postprandial triglyceridemia, seemed to be related to FFA production during lipolysis of triglyceride-rich lipoproteins that were generated in response to fat intake. Postheparin plasma lipoprotein lipase activity was lower in patients, which could offer one explanation why factor VII activity was lower during alimentary lipemia in these subjects despite their exaggerated postprandial triglyceridemia. Thus, activation of coagulation factor VII during alimentary lipemia may result in a procoagulant state that is likely to promote the formation of a coronary thrombus in individuals with established coronary artery disease.
饮食研究已证实血浆脂蛋白与凝血因子VII之间存在联系。本研究旨在具体检测在饮食性脂血症期间凝血因子VII是否被激活,并研究凝血因子VII的质量和活性状态与空腹及餐后脂蛋白和游离脂肪酸(FFA)之间的关系。因此,对33名年轻时曾患心肌梗死的男性(平均年龄±标准差,48.8±3.2岁)和10名年龄匹配的健康对照者,在摄入标准化的混合餐型口服脂肪负荷前后采集的血浆样本中测定了凝血因子VII水平。采用一组凝血因子VII测定方法,以确保能涵盖饮食性脂血症期间该因子所有可能存在形式的变化。结果发现,在饮食性脂血症期间凝血因子VII会发生显著激活,而凝血因子VII分子数量在试餐后保持恒定甚至似乎有所减少。凝血因子VII的激活在对照者中比患者中更明显,且对照者中被激活的凝血因子VII分子比例更高。有趣的是,凝血因子VII的激活与餐后甘油三酯血症程度呈定量相关,似乎与富含甘油三酯脂蛋白在脂肪摄入后脂解过程中产生的游离脂肪酸生成有关。患者的肝素后血浆脂蛋白脂肪酶活性较低,这可以解释为什么尽管这些患者餐后甘油三酯血症加剧,但在饮食性脂血症期间其凝血因子VII活性却较低。因此,饮食性脂血症期间凝血因子VII的激活可能导致促凝状态,这很可能会促进已患冠状动脉疾病个体形成冠状动脉血栓。