Efstathiou Stamatis P, Skeva Irini I, Dimas Cleanthi, Panagiotou Anna, Parisi Kleo, Tzanoumis Labros, Kafouri Anna, Bakratsas Konstantinos, Mountokalakis Theodore D
Center for Cardiovascular Disease Prevention, 'Hygeias Melathron', Athens, Greece.
Atherosclerosis. 2009 Aug;205(2):632-6. doi: 10.1016/j.atherosclerosis.2009.01.022. Epub 2009 Jan 24.
Smoking has been associated with low serum levels of adiponectin, an adipocytokine with insulin-sensitizing, anti-inflammatory and anti-atherogenic properties. The objective of this study was to assess the early effect on adiponectin levels of smoking cessation supported by bupropion.
Apparently healthy smokers of both sexes with no additional cardiovascular risk factors were administered 150mg sustained-release bupropion twice daily for 9 weeks. Quitters constituted the active group and non-quitters the control group. Sandwich enzyme-linked immunosorbent assays were employed for the measurement of serum adiponectin and cotinine, the latter used for validation of self-reported abstinence.
Among the 106 participants (mean age 44.5+/-11.3 years, 57 females, Brinkman index 512.2+/-98.4, basal adiponectin 7.2+/-1.5mg/L), 45 (42.5%) had quitted smoking at week 9. Quitters' post-cessation adiponectin levels were significantly increased (mean difference with baseline 1.9+/-0.8mg/L, 95% CI 1.2, 2.3; p<0.001), while non-quitters' adiponectin remained unaltered. A multiple regression model including female gender (standardized beta coefficient=0.480, p=0.002), age (0.355, p=0.003), body mass index (BMI) (-0.308, p=0.005), waist circumference (-0.276, p=0.008), smoking status (-0.255, p=0.010), and cotinine levels (-0.233, p=0.021) explained about two thirds of the variation in adiponectin levels (adjusted R(2)=0.656).
Serum adiponectin levels appear to increase considerably within 2 months after smoking cessation. This finding may provide further insight into the mechanisms related to the detrimental effects of smoking and the benefits of quitting.
吸烟与血清脂联素水平降低有关，脂联素是一种具有胰岛素增敏、抗炎和抗动脉粥样硬化特性的脂肪细胞因子。本研究的目的是评估安非他酮支持下戒烟对脂联素水平的早期影响。
对无其他心血管危险因素的明显健康的男女吸烟者，每日两次给予150mg缓释安非他酮，持续9周。戒烟者组成治疗组，未戒烟者组成对照组。采用夹心酶联免疫吸附测定法测量血清脂联素和可替宁，后者用于验证自我报告的戒烟情况。
106名参与者（平均年龄44.5±11.3岁，57名女性，Brinkman指数512.2±98.4，基础脂联素7.2±1.5mg/L）中，45名（42.5%）在第9周戒烟。戒烟者戒烟后的脂联素水平显著升高（与基线的平均差异为1.9±0.8mg/L，95%CI为1.2，2.3；p<0.001），而未戒烟者的脂联素水平保持不变。一个多元回归模型，包括女性性别（标准化β系数=0.480，p=0.002）、年龄（0.355，p=0.003）、体重指数（BMI）（-0.308，p=0.005）、腰围（-0.276，p=0.008）、吸烟状态（-0.255，p=0.010）和可替宁水平（-0.233，p=0.021），解释了脂联素水平约三分之二的变化（调整后R²=0.656）。
戒烟后2个月内血清脂联素水平似乎显著升高。这一发现可能为深入了解吸烟的有害影响和戒烟的益处相关机制提供进一步的线索。
