Finding
Thus, TNF-alpha may contribute to the insulin resistance of overall obesity, whereas IL-6 may be one of the mediators of the hyperinsulinemic state specifically related to excess visceral adiposity.
Paper
Visceral obesity and plasma glucose-insulin homeostasis: contributions of interleukin-6 and tumor necrosis factor-alpha in men.
Abstract
OBJECTIVE This study examined the relationships of two inflammatory cytokines, IL-6 and TNF-alpha, to visceral adiposity and indices of plasma glucose-insulin homeostasis. RESEARCH DESIGN AND METHODS Plasma levels of IL-6 and TNF-alpha were measured in 189 untreated asymptomatic men (aged 43.7 +/- 7.8 yr; body mass index 29.0 +/- 4.3 kg/m(2); waist girth 98.6 +/- 10.3 cm). RESULTS Significant and positive associations were found between both cytokines with adiposity and adipose tissue distribution indices (0.15 < or = r < 0.32; P < 0.05) as well as plasma glucose-insulin homeostasis variables (0.22 < or = r < 0.28; P <0.05). Comparison of two subgroups, each composed of 32 overweight men (> or =25 kg/m(2)) with similar body mass index values (28.7 kg/m(2) in both groups) but with markedly different levels of visceral adipose tissue (< vs. > or = 130 cm(2)), revealed significant differences only for IL-6 levels (1.42 +/- 1.15 vs. 0.86 +/- 0.52 pg/ml; P < 0.02 for men with high vs. low visceral adipose tissue, respectively). Finally, when subjects were stratified on the basis of their respective concentrations of IL-6 and TNF-alpha (using the 50th percentile of their overall distribution), an ANOVA revealed an independent contribution of IL-6 to the variation of fasting insulin (P < 0.01) and each of these two cytokines to the variation of insulin levels measured after a 75-g oral glucose challenge (P <0.01 for IL-6 and P < 0.05 for TNF-alpha). CONCLUSIONS Because IL-6 appeared to be clearly associated with visceral adiposity, TNF-alpha rather showed associations with indices of total body fatness. Thus, TNF-alpha may contribute to the insulin resistance of overall obesity, whereas IL-6 may be one of the mediators of the hyperinsulinemic state specifically related to excess visceral adiposity.
Authors
A. Cartier, I. Lemieux, N. Alméras
Journal
The Journal of clinical endocrinology and metabolism