Background: Obesity is associated with an increased risk of impaired glucose tolerance and type 2 diabetes. Insulin resistance is the link between obesity and disturbances of glucose metabolism. It is suggested that some substances secreted by adipose tissue might play a role in the pathogenesis of insulin resistance. One of these substances is interleukin-6 (IL-6), cytokine, which regulates synthesis of the acute-phase proteins in the liver. The aim of the present study was to estimate serum IL-6, soluble form of IL-6 receptor (sIL6-R) and C-reactive protein concentrations (hs-CRP) in obese subjects with normal and impaired glucose tolerance.
Methods: The study group consisted of 107 subjects, 28 obese with impaired glucose tolerance (IGT), 44 obese with normal glucose tolerance (obese-NGT) and 35 lean healthy controls. Insulin sensitivity was measured with euglycemic hyperinsulinemic clamp technique. The protocol was approved by Ethics Committee of Medical University, and informed consent was obtained from each subject.
Results: IGT subjects had lower insulin sensitivity index in comparison to obese-NGT and controls (both P<0.000001), and obese-NGT subjects had lower insulin sensitivity in comparison to controls (P=0.00043). We found higher IL-6 and hs-CRP concentrations in IGT group in comparison to obese-NGT (P=0.042 and P=0.041 respectively) and to controls (P=0.00056 and P<0.000001 respectively). Differences in sIL-6R concentration between IGT subjects and the remaining groups were approaching the level of significance (obese-NGT, P=0.087, control, P=0.066). We found significant correlations between insulin sensitivity index and IL-6 (r=−0.21, P=0.029), sIL-6R (r=−0.19, P=0.049) and hs-CRP (r=−0.34, P=0.001). IL-6, sIL-6R and hs-CRP were also associated with fasting insulin and with post load glucose and insulin concentrations. IL-6 and hs-CRP were also related to triglycerides and HbA1c and IL-6 was related to HDL-cholesterol.
Conclusions: Our data indicate that IL-6/sIL-6R system might play a role in the development of insulin resistance in obese subjects with IGT.