Evaluation of insulin resistance, tumor necrosis factor alpha, and total antioxidant status in obese patients smoking cigarettes.

INTRODUCTION AND
BACKGROUND: Obesity and smoking are leading causes of morbidity and mortality worldwide. Cross-sectional studies indicate that heavy smoking may be associated with a greater risk of obesity. While there are important unresolved issues in relation to the effect of smoking on body weight, there is increasing evidence that smoking is conducive to a greater accumulation of visceral fat and greater insulin resistance. AIM: of this study was to determine the potential influences of obesity and smoking on tumor necrosis factor alpha (TNF-α), total antioxidant status (TAS), and insulin resistance. SUBJECTS AND METHODS: 30 obese nonsmokers, 30 obese smokers, 30 normal-weight smokers, and 30 healthy volunteers (the control) were studied. In all subjects, assessments of TNF-α, TAS, and insulin were made. Insulin resistance was evaluated according to the homeostasis model assessment-insulin resistance (HOMA-IR) protocol.
RESULTS: TNF-α concentrations, as well as insulin resistance levels, in obese patients significantly exceeded those observed in the control. Compared to the control, obese patients presented significantly lower TAS levels. In the group of obese patients who actively smoked cigarettes, further increases in TNF-α and insulin resistance, as well as decreases in TAS level, were noticed. TNF-α concentration and insulin resistance levels were significantly higher, while TAS was lower in normal-weight smoking subjects, compared to the control. A positive correlation between TNF-α and HOMA-IR was found in the overall population.
CONCLUSIONS: Obesity may evoke inflammatory processes, oxidative stress, and insulin resistance, all of which are aggravated by cigarette smoking. TNF-α should be considered in the complex pathogenesis of insulin resistance in obese patients who actively smoke.