Freeman D J, Griffin B A, Murray E, Lindsay G M, Gaffney D, Packard C J, Shepherd J
Institute of Biochemistry, Royal Infirmary, Glasgow, UK.
Eur J Clin Invest. 1993 Oct;23(10):630-40. doi: 10.1111/j.1365-2362.1993.tb00724.x.
In a survey of a healthy population (n = 197), LDL cholesterol, plasma triglycerides and VLDL triglycerides were found to be substantially increased and plasma HDL cholesterol decreased in smokers. The lipid-associated atherogenic risk in smokers as assessed by the LDL/HDL ratio was significantly higher [2.89 (SD 1.18, n = 63)] than in non-smokers [2.38 (SD 0.98, n = 86) P < 0.01]. The lower HDL level found in smokers was explained by a lower HDL-2 subfraction as determined by analytical ultracentrifugation. HDL 2b, 2a and 3a, measured by gradient gel electrophoresis, were all lower in the smokers but this was only significant for HDL 2a. Smoking had no effect on Lp(a) levels. HDL cholesterol and HDL-2 were strongly negatively correlated whereas LDL cholesterol and LDL/HDL ratio were strongly positively correlated with the plasma triglyceride concentration. There was a small but significant reduction in plasma CETP activity [non-smokers 49% t/microliter (SD 17, n = 90), smokers 43% t/microliter (SD 17, n = 66) P < 0.05] but CETP activity was not correlated with any measure of HDL in this population. Smoking was found to be an important independent contributor to the variation in plasma triglyceride, HDL, HDL-2 and LDL/HDL ratio. After correcting for sex, age, BMI, alcohol consumption, oral contraceptive use and plasma triglycerides smoking was still found to be significantly associated with HDL and the LDL/HDL ratio. Upon adjustment for covariant factors the mean differences between smokers and non-smokers for HDL cholesterol, HDL-2 and LDL/HDL were 0.15 mM, 16 mg dl-1 and 0.39 respectively. There appeared to be important sex differences in the influence of smoking on plasma lipoproteins. In women the main impact of smoking was on triglyceride levels and they in turn affected LDL and HDL. In contrast, in men, smoking had little impact on triglycerides and affected HDL more directly. We conclude that smoking cigarettes has an important effect on plasma lipoprotein metabolism through multiple mechanisms.
在一项对健康人群(n = 197)的调查中,发现吸烟者的低密度脂蛋白胆固醇、血浆甘油三酯和极低密度脂蛋白甘油三酯显著升高,而血浆高密度脂蛋白胆固醇降低。通过低密度脂蛋白/高密度脂蛋白比值评估,吸烟者的脂质相关动脉粥样硬化风险[2.89(标准差1.18,n = 63)]显著高于非吸烟者[2.38(标准差0.98,n = 86),P < 0.01]。吸烟者中发现的较低高密度脂蛋白水平是由分析超速离心法测定的较低高密度脂蛋白2亚组分所解释的。通过梯度凝胶电泳测量的高密度脂蛋白2b、2a和3a在吸烟者中均较低,但仅高密度脂蛋白2a有显著差异。吸烟对脂蛋白(a)水平无影响。高密度脂蛋白胆固醇与高密度脂蛋白2呈强烈负相关,而低密度脂蛋白胆固醇和低密度脂蛋白/高密度脂蛋白比值与血浆甘油三酯浓度呈强烈正相关。血浆胆固醇酯转运蛋白(CETP)活性有小幅但显著的降低[非吸烟者49% t/微升(标准差17,n = 90),吸烟者43% t/微升(标准差17,n = 66),P < 0.05],但在该人群中,CETP活性与任何高密度脂蛋白指标均无相关性。发现吸烟是血浆甘油三酯、高密度脂蛋白、高密度脂蛋白2和低密度脂蛋白/高密度脂蛋白比值变化的重要独立因素。在校正性别、年龄、体重指数、饮酒量、口服避孕药使用情况和血浆甘油三酯后,仍发现吸烟与高密度脂蛋白和低密度脂蛋白/高密度脂蛋白比值显著相关。在调整协变量因素后,吸烟者与非吸烟者在高密度脂蛋白胆固醇、高密度脂蛋白2和低密度脂蛋白/高密度脂蛋白方面的平均差异分别为0.15 mM、16 mg/dl和0.39。吸烟对血浆脂蛋白的影响似乎存在重要的性别差异。在女性中,吸烟的主要影响是对甘油三酯水平,进而影响低密度脂蛋白和高密度脂蛋白。相比之下,在男性中,吸烟对甘油三酯影响较小,对高密度脂蛋白影响更直接。我们得出结论,吸烟通过多种机制对血浆脂蛋白代谢有重要影响。