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This version published online on March 4, 2008
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2007-2191
A more recent version of this article appeared on May 1, 2008
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Submitted on October 1, 2007
Accepted on February 26, 2008

Visceral obesity and plasma glucose-insulin homeostasis: contributions of IL-6 and TNF-{alpha} in men

Amélie Cartier MSc, Isabelle Lemieux PhD, Natalie Alméras PhD, Angelo Tremblay PhD, Jean Bergeron MD, MSc, and Jean-Pierre Després PhD, FAHA*

Québec Heart Institute, Hôpital Laval Research Centre, Hôpital Laval, Québec (Qc), Canada; Department of Anatomy and Physiology, Université Laval, Québec (Qc), Canada; Lipid Research Centre, CHUL Research Centre, Québec (Qc), Canada; Division of Kinesiology, Department of Social and Preventive Medicine, Université Laval, Québec (Qc), Canada

* To whom correspondence should be addressed. E-mail: jean-pierre.despres{at}crhl.ulaval.ca.

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 (age: 43.7±7.8 years; body mass index (BMI): 29.0±4.3 kg/m2; 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≤r<0.32; p<0.05) as well as with plasma glucose-insulin homeostasis variables (0.22≤r<0.28; p<0.05). Comparison of two subgroups each composed of 32 overweight men (≥25 kg/m2) with similar BMI values (28.7 kg/m2 in both groups) but with markedly different levels of visceral adipose tissue (< vs. ≥130 cm2) 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 analysis of variance revealed an independent contribution of IL-6 to the variation of fasting insulin (p<0.01) and of each of these two cytokines to the variation of insulin levels measured following a 75g oral glucose challenge (p<0.01 for IL-6 and p<0.05 for TNF-{alpha}).

Conclusions: As 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.


Key words: Abdominal obesity • adipokines • hyperinsulinemia • inflammation







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