Plasma soluble tumour necrosis factor-alpha receptor 2 is elevated in obesity: specific contribution of visceral...

We examined the obesity phenotype most strongly associated with increased plasma concentrations of sTNFR2, and compared which of the two markers, TNF-alpha or sTNFR2, better predicts indices of plasma glucose-insulin homeostasis.

Plasma sTNFR2 levels were measured in a sample of 287 healthy nondiabetic men [age: 43.9 +/- 8.0 years (mean +/- SD)], covering a wide range of adiposity values (BMI: 29.0 +/- 4.4 kg/m(2); waist girth: 100.0 +/- 11.7 cm).

Plasma sTNFR2 levels correlated positively and significantly with BMI (r = 0.36; P < 0.0001), fat mass (r = 0.42; P < 0.0001), waist girth (r = 0.38; P < 0.0001) as well as with visceral (r = 0.37; P < 0.0001) and subcutaneous adipose tissue (AT) (r = 0.40; P < 0.0001) areas measured by computed tomography. Two subgroups (n = 27 in each group) of overweight men (BMI >or=25 kg/m(2)) were individually matched for similar BMI values, but with markedly different levels of visceral AT (< or >or=130 cm(2)) and then compared with a control group of 46 lean subjects (with both BMI <25 kg/m(2) and visceral AT <130 cm(2)). This analysis revealed that men characterized by high levels of visceral AT had significantly higher concentrations of sTNFR2 compared with obese men with low visceral AT (1861 +/- 457 pg/ml vs. 1722 +/- 400; P < 0.05) and with lean controls (1570 +/- 291 pg/ml; P < 0.001). Whereas subjects classified across tertiles of TNF-alpha levels showed no difference in glucose tolerance and insulin levels, subjects in the upper tertile of plasma sTNFR2 levels were characterized with the highest plasma insulin concentrations during the OGTT and had the highest area under the curve of insulin concentrations.

These results indicate that sTNFR2 levels are more closely related to abdominal AT accumulation than to total adiposity. Furthermore, plasma concentrations of sTNFR2 are independently related to plasma glucose-insulin homeostasis beyond the known contribution of visceral adiposity.