Obesity is associated with subclinical, chronic, and systemic immune activation characterized by increased serum concentration of proinflammatory cytokines released by adipose tissue. The aim of the present study was to determine the relationship between stage of development of obesity and changes in activity of tumor necrosis factor (TNF) system during 5-year follow-up observation. One hundred fifty-four women--102 obese, 24 overweight, and 28 lean--without concomitant diseases were examined for the first time from 2000 to 2001. After 5 years, 57 obese, 12 overweight, and 14 lean subjects were reexamined. In addition to anthropometric measurements, body composition was determined by the bioimpedance method; and serum concentrations of glucose, lipids, insulin, TNF-α, and soluble TNF receptors (sTNFRs) were measured. Only reexamined subjects were included in the analysis. After 5 years, fat mass increased significantly in 46 (66.7%) overweight or obese women and in all lean subjects (39.0 ± 12.3 vs 47.3 ± 13.6 kg, P < .001; 14.8 ± 3.7 vs 20.6 ± 5.4 kg, P < .01, respectively), whereas it decreased in 23 (33.3%) overweight or obese subjects (41.3 ± 12.5 vs 37.2 ± 14.0 kg, P < .005). The TNF-α levels increased significantly only in lean women (3.1 ± 3.0 vs 5.6 ± 2.0 pg/mL, P < .005), but remained unchanged in overweight and obese subjects regardless of fat mass changes. Serum concentrations of sTNFR1 and sTNFR2 decreased by 71% and 25% in obese, by 104% and 21% in overweight, and by 31% and 32% in lean group, respectively. The increase of plasma TNF-α level is an early event in abdominal fat accumulation. It seems that further fat mass gain does not enhance circulating TNF-α levels.
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