ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P576

Hypoadiponectinemia but not activation of immune markers is associated with impaired glucose metabolism in morbidly obese patients

Sven Schinner, Kerstin Kempf, Hubert Overmann, Thomas Rotthoff, Matthias Schott, Bettina Rose, Werner A Scherbaum & Christian Herder


University Hospital, Dusseldorf, Germany.


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.

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