Objectives: Obesity is the major risk factor for the development of impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). In addition, increased circulating levels of cytokines and chemokines and decreased adiponectin levels are associated with IGT and T2DM. However, a large part of morbidly obese patient remain normoglycemic. Therefore, we investigated if this protection can be attributed to a lower grade of inflammation or higher adiponectin levels.
Methods: Glucose tolerance of morbidly obese patients (n=2754, body mass index ≥40 kg/m2) was assessed by oral glucose tolerance tests. In a case-control design we compared levels of eight immune mediators and adiponectin from patients with IGT/T2DM (n=52) and normal glucose tolerance (NGT; n=59). Gene expression in peripheral blood was determined by quantitative RT-PCR, and serum concentrations of immune mediators and adiponectin were measured by ELISA and bead-based multiplex technology.
Results: About 54% of the patients in our morbidly obese cohort were normoglycaemic, while 14% were diagnosed with IGT and 32% with T2DM. There was no statistically significant difference in mRNA expression or serum levels of proinflammatory markers. Interestingly, we could demonstrate an association of NGT with higher adiponectin levels (P=0.039). Adiponectin levels were negatively correlated with interleukin (IL)-6 and macrophage chemoattractant protein (MCP)-1, but independent the other immune mediators.
Conclusions: Lower adiponectin levels were associated with IGT/T2DM, but there was no further increase in inflammatory markers with IGT/T2DM in morbid obesity. This suggests that in addition to chronic, low-grade inflammation, adiponectin is an important factor in the development of, or protection against, T2DM in obesity.
03 - 07 May 2008
European Society of Endocrinology