Influence of smoking and body weight on adipokines in middle aged women

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-α 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 μg/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-α. 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 μg/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).