Farin H M F, Abbasi F, Kim S H, Lamendola C, McLaughlin T, Reaven G M
Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Diabetes Obes Metab. 2007 Jan;9(1):65-9. doi: 10.1111/j.1463-1326.2006.00574.x.
Considerable evidence shows that cigarette smokers tend to have the dyslipidemic pattern of high plasma triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) concentrations, a highly atherogenic lipoprotein profile also typical of the insulin-resistant state even in the absence of cigarette smoking. However, because cigarette smokers are frequently insulin resistant, it is unclear if this dyslipidaemia is secondary to smoking, per se, or simply to the fact that smokers tend to be insulin resistant. The present study was initiated to determine whether this dyslipidaemia prevalent in cigarette smokers and characteristic of insulin-resistant individuals is a function of cigarette smoking or of insulin resistance.
As measured using vertical auto profile-II methodology, the lipid and lipoprotein concentrations were compared in 34 cigarette smokers divided into insulin-sensitive and insulin-resistant subgroups. The two groups were similar in age and body mass index, differing only in their insulin-mediated glucose uptake as quantified by the steady-state plasma glucose concentration determined during the insulin suppression test.
While levels of TG and very low-density lipoprotein cholesterol (VLDL-C) were significantly elevated in insulin-resistant cigarette smokers, total cholesterol (C), low-density lipoprotein cholesterol (LDL-C), narrow-density (ND) LDL-C, intermediate-density lipoprotein-C (IDL-C), HDL-C and non-HDL-C were not different in the two groups. The insulin-resistant smokers also had a preponderance of small, dense LDL particles, while the reverse was true of the insulin-sensitive cigarette smokers.
These data suggest that the dyslipidaemia previously attributed to smoking occurs primarily in those smokers who are also insulin resistant.
大量证据表明，吸烟者往往具有血浆甘油三酯（TG）升高和高密度脂蛋白胆固醇（HDL-C）浓度降低的血脂异常模式，即使在不吸烟的情况下，这种高度致动脉粥样硬化的脂蛋白谱也是胰岛素抵抗状态的典型特征。然而，由于吸烟者经常存在胰岛素抵抗，目前尚不清楚这种血脂异常是继发于吸烟本身，还是仅仅因为吸烟者往往存在胰岛素抵抗。本研究旨在确定吸烟者中普遍存在的、胰岛素抵抗个体所特有的这种血脂异常是吸烟的作用还是胰岛素抵抗的作用。
采用垂直自动分析仪-II方法进行测量，比较了34名吸烟者分为胰岛素敏感和胰岛素抵抗亚组后的脂质和脂蛋白浓度。两组在年龄和体重指数方面相似，仅在胰岛素抑制试验期间通过稳态血浆葡萄糖浓度量化的胰岛素介导的葡萄糖摄取方面有所不同。
虽然胰岛素抵抗的吸烟者中TG和极低密度脂蛋白胆固醇（VLDL-C）水平显著升高，但两组的总胆固醇（C）、低密度脂蛋白胆固醇（LDL-C）、窄密度（ND）LDL-C、中密度脂蛋白-C（IDL-C）、HDL-C和非HDL-C并无差异。胰岛素抵抗的吸烟者还存在大量小而密的LDL颗粒，而胰岛素敏感的吸烟者则相反。
这些数据表明，先前归因于吸烟的血脂异常主要发生在那些同时存在胰岛素抵抗的吸烟者中。
