Freeman D J, Caslake M J, Griffin B A, Hinnie J, Tan C E, Watson T D, Packard C J, Shepherd J
Institute of Biochemistry, Royal Infirmary, Glasgow, UK.
Eur J Clin Invest. 1998 Jul;28(7):584-91. doi: 10.1046/j.1365-2362.1998.00328.x.
Smoking is associated with dyslipidaemia, particularly raised plasma triglycerides and reduced high-density lipoprotein (HDL)-cholesterol and a delayed clearance of triglyceride in fat tolerance tests. The aim of this study was to investigate whether these phenomena could be explained by a reduced lipoprotein lipase activity in smokers.
A group of 40 healthy individuals [plasma cholesterol 5.07 (SD 0.90) mmol L-1, plasma triglyceride 1.02 (SD 0.39) mmol L-1)] was studied to examine the effects of smoking on plasma enzyme activities, particularly post-heparin lipase activities. The group comprised 20 smokers and 20 non-smokers, who were matched for age, gender and body mass index (BMI).
Post-heparin lipoprotein lipase (LPL) activity [3.89 (SD 1.58) vs. 5.85 (SD 2.30) mumol free fatty acids (FFA) mL-1 h-1, P < 0.005], but not post-heparin hepatic lipase (HL) activity, was reduced in smokers. Plasma cholesteryl ester transfer protein (CETP) activity and lecithin: cholesterol acyl transferase (LCAT) activity were measured in a subgroup of 18 individuals, comprising nine smokers with nine matched non-smokers. There was no difference in CETP activities between two groups, but smokers had a significantly reduced plasma LCAT activity [112 (SD 23) vs. 152 (SD 24) nmol cholesterol mL-1 h-1, P < 0.005]. In both smokers (r=-0.53, P < 0.05) and non-smokers (r=-0.54, P < 0.05), HDL2 concentration was negatively associated with HL activity. In non-smokers, HDL3 concentration was negatively associated with CETP activity (r= -0.77, P < 0.05), whereas in smokers HDL3 concentration was negatively associated with LCAT activity (r= -0.78, P < 0.050).
It was shown by direct measurement that the activity of plasma post-heparin LPL is reduced in smokers, independently of age, gender and BMI. It is concluded that this enzyme perturbation associated with smoking may contribute to the development of the atherogenic lipoprotein phenotype seen in smokers.
吸烟与血脂异常有关，尤其是血浆甘油三酯升高、高密度脂蛋白（HDL）胆固醇降低，以及脂肪耐量试验中甘油三酯清除延迟。本研究的目的是调查这些现象是否可以用吸烟者脂蛋白脂肪酶活性降低来解释。
对一组40名健康个体[血浆胆固醇5.07（标准差0.90）mmol/L，血浆甘油三酯1.02（标准差0.39）mmol/L]进行研究，以检查吸烟对血浆酶活性的影响，特别是肝素后脂肪酶活性。该组包括20名吸烟者和20名不吸烟者，他们在年龄、性别和体重指数（BMI）方面相匹配。
吸烟者肝素后脂蛋白脂肪酶（LPL）活性降低[3.89（标准差1.58）对5.85（标准差2.30）μmol游离脂肪酸（FFA）/mL-1/h-1，P<0.005]，但肝素后肝脂肪酶（HL）活性未降低。在一个由18名个体组成的亚组中测量了血浆胆固醇酯转移蛋白（CETP）活性和卵磷脂：胆固醇酰基转移酶（LCAT）活性，该亚组包括9名吸烟者和9名匹配的不吸烟者。两组之间的CETP活性没有差异，但吸烟者的血浆LCAT活性显著降低[112（标准差23）对152（标准差24）nmol胆固醇/mL-1/h-1，P<0.005]。在吸烟者（r=-0.53，P<0.05）和不吸烟者（r=-0.54，P<0.05）中，HDL2浓度均与HL活性呈负相关。在不吸烟者中，HDL3浓度与CETP活性呈负相关（r=-0.77，P<0.05），而在吸烟者中，HDL3浓度与LCAT活性呈负相关（r=-0.78，P<0.050）。
通过直接测量表明，吸烟者血浆肝素后LPL活性降低，与年龄、性别和BMI无关。得出的结论是，这种与吸烟相关的酶紊乱可能有助于吸烟者出现动脉粥样硬化脂蛋白表型。
