INSULIN RESISTANCE AND CIGARETTE-SMOKING
INSULIN RESISTANCE AND CIGARETTE-SMOKING
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DOI：
10.1016/0140-6736(92)90730-q
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发表时间：
1992-05-09
期刊：
影响因子：
168.9
通讯作者：
REAVEN, GM
中科院分区：
文献类型：
--
作者：
FACCHINI, FS;HOLLENBECK, CB;REAVEN, GM
吸烟与血浆甘油三酯升高和血浆高密度脂蛋白胆固醇浓度降低有关。这些变化不仅增加冠心病的风险，而且继发于胰岛素刺激的葡萄糖摄取抵抗或高胰岛素血症。为了了解吸烟与胰岛素介导的葡萄糖摄取之间是否存在关系，我们测量了40名匹配的健康志愿者（20名不吸烟者，20名吸烟者）的血浆脂质和脂蛋白浓度、口服葡萄糖刺激时的血浆葡萄糖和胰岛素反应，以及胰岛素介导的葡萄糖摄取。吸烟者的极低密度脂蛋白甘油三酯（0.66 [0.10]vs 0.39 [0.03] mmol/l, p < 0.02）和胆固醇（0.45 [0.06]vs 0.23 [0.04] mmol/l, p < 0.005）的平均浓度显著升高，高密度脂蛋白胆固醇（1.16 [0.05]vs 1.51 [0.08]mmol/l, p < 0.001）浓度显著降低。尽管两组的血浆葡萄糖浓度对口服葡萄糖负荷的反应相似，但吸烟者的血浆胰岛素反应明显更高（p < 0.001）。最后，吸烟者在连续输注葡萄糖、胰岛素和生长抑素后，稳态血浆葡萄糖浓度更高（8.4 [0.2]vs 5.0 [0.3] mmol/l, p < 0.001），尽管稳态血浆胰岛素浓度相似。研究结果表明，与不吸烟者相比，慢性吸烟者有胰岛素抵抗、高胰岛素血症和血脂异常，这可能有助于解释为什么吸烟会增加患冠心病的风险。
Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers).Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0.66 [0.10] vs 0.39 [0.03] mmol/l, p < 0.02) and cholesterol (0.45 [0.06] vs 0.23 [0.04] mmol/l, p < 0.005) concentrations and lower high-density-lipoprotein cholesterol concentrations (1.16 [0.05] vs l.51 [0.08]mmol/l, p < 0.001). Although plasma glucose concentrations in response to the oral glucose load were similar in the two groups, plasma insulin response of the smokers was significantly higher (p < 0.001). Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p < 0.001), despite similar steady-state plasma insulin concentrations.The findings show that chronic cigarette smokers are insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of coronary heart disease.