The insulin resistance syndrome and postprandial lipid intolerance in smokers
The insulin resistance syndrome and postprandial lipid intolerance in smokers
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DOI：
10.1016/s0021-9150(96)06028-5
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发表时间：
1997-02-28
期刊：
影响因子：
5.3
通讯作者：
Smith, U
中科院分区：
文献类型：
--
作者：
Eliasson, B;Mero, N;Smith, U
背景：研究吸烟对健康中年男性胰岛素抵抗、餐后混合餐后血脂、脂蛋白等胰岛素抵抗综合征（IRS）的影响。方法：36名吸烟男性和25名年龄和体重指数（BMI）匹配的非吸烟男性参与研究。他们均为非肥胖（BMI < 27）、健康且未服用任何药物。吸烟者每天吸烟超过10支，持续时间超过20年；非吸烟者从来都不是习惯性吸烟者。研究了身体组成和几种代谢和心血管危险因素，包括混合餐后小密度ldl颗粒、脂蛋白和肝脂肪酶活性以及甘油三酯水平的流行。胰岛素敏感性的测定采用正糖高胰岛素钳夹技术。结果：吸烟者的hdl -胆固醇和脂蛋白A-I水平较低，但空腹甘油三酯较高，小密度ldl颗粒比例增加，肝素后脂肪酶活性较高。在钳夹期间，他们的纤维蛋白原、纤溶酶原激活物抑制剂1 （PAI-1）活性、空腹和稳态c肽水平也较高。吸烟者在混合试验餐后出现胰岛素抵抗和脂质不耐受，甘油三酯清除受损。这种脂质不耐受在空腹高甘油三酯血症中没有反映出来。结论：本研究采用正糖高胰岛素钳夹技术，显示吸烟者同时存在胰岛素抵抗和脂质不耐受。餐后脂质不耐受也见于空腹甘油三酯水平正常的个体，并与致动脉粥样硬化小密度LDL的患病率增加有关。IRS可能是吸烟者心血管发病率增加的一个重要原因。(C) 1997爱思唯尔科学爱尔兰有限公司
Background: The effects of cigarette smoking on insulin resistance, postprandial lipemia following a mixed meal, lipoproteins and other aspects of the insulin resistance syndrome (IRS) were investigated in healthy middle-aged men. Methods: 36 smoking and 25 age- and body mass index (BMI)-matched non-smoking men participated. They were non-obese (BMI < 27), healthy and without any medication. The smokers had been smoking more than 10 cigarettes per day for more than 20 years; the non-smokers had never been habitual smokers. Body composition and several metabolic and cardiovascular risk factors were studied, including the prevalence of small dense LDL-particles, lipoprotein and hepatic lipase activity and triglyceride levels after a mixed lest meal. For determination of degree of insulin sensitivity the euglycemic hyperinsulinemic clamp technique was used. Results: The smokers had lower HDL-cholesterol and lipoprotein A-I levels but higher fasting triglycerides, as well as an increased proportion of small dense LDL-particles and higher postheparin hepatic lipase activity. They also had higher levels of fibrinogen, plasminogen activator inhibitor 1 (PAI-1) activity and fasting and steady-state C-peptide levels during the clamp. The smokers were insulin resistant and lipid intolerant with an impaired triglyceride clearance after a mixed test meal. This lipid intolerance was not mirrored by fasting hypertriglyceridemia. Conclusions: This study, using the euglycemic hyperinsulinemic clamp technique, shows that smokers are both insulin resistant and lipid intolerant. The postprandial lipid intolerance is also seen in individuals with normal fasting triglyceride levels and is related to an increased prevalence of atherogenic small dense LDL. IRS is likely to be an important reason for the increased cardiovascular morbidity in smokers. (C) 1997 Elsevier Science Ireland Ltd.