Technische Universität Dresden, Universitätsklinikum Carl Gustav Carus, Institut für Klinische Chemie und Laboratoriumsmedizin, Dresden, Germany.
Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):21-6. doi: 10.1186/2047-783x-14-s4-21.
Quitting smoking was associated with an undesirable weight gain. Both, cigarette smoking and obesity were accompanied by subclinical systemic inflammation. This may cause unfavourable changes in (plasma) adipokine concentration. The aim of the present study was to establish the influence of moderate cigarette smoking on the concentration of the adipokines leptin and adiponectin and the pro-inflammatory factors CRP, SAA, IL-6 and TNF-a in non-obese (n=138) and obese (n=175) perimenopausal women of the DRECAN-2005 survey.
Among non-obese women, adiponectin was significantly lower in smokers than in non-smokers (16.88 +/-6.85 vs. 20.63 +/-10.04 microg/ml; P<0.05). Leptin tended to lower values, too. Among obese women, none significant differences in adiponectin or leptin concentration were observed between smokers and non-smokers. In obese smokers and obese non-smokers, the adiponectin concentrations were significantly lower and the leptin concentrations were significantly higher than in non-obese non-smokers. Non-obese smokers showed significantly higher leukocyte count (6.50 +/- 1.83 vs. 5.51 +/- 1.31 GPT/l; P<0.001) and serum amyloid A concentration (7.81 +/- 1.25 vs. 4.22 +/- 1.43 mg/l; P<0.05) than non-obese non-smokers. There were only tendencies to higher concentration of CRP, IL-6, and TNF-alpha. In obese women, moderate cigarette smoking was not associated with higher leukocyte count or concentration of SAA. Among non-smokers, overweight was associated higher concentration of leptin (22.16 +/- 12.16 vs. 11.49 +/- 6.37 ng/ml; P<0.001) and with significantly lower concentration of adiponectin (16.29 +/- 8.01 vs. 20.77 +/- 9.99 microg/ml; P<0.001). Among smokers, overweight was associated with higher leptin concentration only (obese: 18.62 +/- 13.46 vs. non-obese: 8.84 +/- 4.92 ng/ml; P<0.01).
In non-obese middle aged women, even moderate cigarette smoking adversely influences the serum concentration of adiponectin and SAA. Overweight hides possible effects of smoking on cytokines and adipokines.
戒烟与不良的体重增加有关。吸烟和肥胖都伴随着亚临床系统性炎症。这可能导致（血浆）脂肪因子浓度的不利变化。本研究的目的是确定适度吸烟对非肥胖（n=138）和肥胖（n=175）绝经前妇女中瘦素和脂联素等脂肪因子以及 CRP、SAA、IL-6 和 TNF-a 等促炎因子浓度的影响。
在非肥胖女性中，吸烟者的脂联素明显低于不吸烟者（16.88±6.85 与 20.63±10.04 μg/ml；P<0.05）。瘦素也有降低的趋势。在肥胖女性中，吸烟者和不吸烟者的脂联素或瘦素浓度无显著差异。在肥胖的吸烟者和肥胖的非吸烟者中，脂联素浓度明显低于非肥胖的非吸烟者，瘦素浓度明显高于非肥胖的非吸烟者。非肥胖的吸烟者的白细胞计数（6.50±1.83 与 5.51±1.31 GPT/l；P<0.001）和血清淀粉样蛋白 A 浓度（7.81±1.25 与 4.22±1.43 mg/l；P<0.05）明显高于非肥胖的非吸烟者。CRP、IL-6 和 TNF-α仅呈升高趋势。在肥胖女性中，中度吸烟与白细胞计数或 SAA 浓度升高无关。在非吸烟者中，超重与较高的瘦素浓度（22.16±12.16 与 11.49±6.37 ng/ml；P<0.001）和较低的脂联素浓度（16.29±8.01 与 20.77±9.99 μg/ml；P<0.001）相关。在吸烟者中，只有超重与较高的瘦素浓度相关（肥胖者：18.62±13.46 与非肥胖者：8.84±4.92 ng/ml；P<0.01）。
在非肥胖的中年女性中，即使是适度的吸烟也会对脂联素和 SAA 的血清浓度产生不良影响。超重掩盖了吸烟对细胞因子和脂肪因子的可能影响。
