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Systemic monocyte chemoattractant protein-1 concentrations are independent of type 2 diabetes or parameters of obesity: results from the Cooperative Health Research in the Region of Augsburg Survey S4 (KORA S4)

German Diabetes Clinic, German Diabetes Centre, Leibniz Centre at Heinrich-Heine-University, Auf’m Hennekamp 65, 40225 Düsseldorf, Germany, ¹ Department of Internal Medicine II-Cardiology, Medical Centre, University of Ulm, Ulm, Germany, ² Institute of Epidemiology, GSF-National Research Centre for Environment and Health, Neuherberg, Germany, ³ Institute of Biometrics and Epidemiology, German Diabetes Centre, Leibniz Centre at Heinrich-Heine-University, Düsseldorf, Germany and ⁴ Institute of Health Economics and Health Care Management, GSF-National Research Centre for Environment and Health, Neuherberg, Germany

(Correspondence should be addressed to C Herder; Email: Christian.Herder{at}ddz.uni-duesseldorf.de)

Objective: Data on the relevance of monocyte chemoattractant protein (MCP)-1 in the pathophysiology of type 2 diabetes (T2D) and obesity are inconsistent. Since MCP-1 is produced by adipocytes and has been postulated to be involved in macrophage infiltration into adipose tissue, we wanted to test whether serum MCP-1 levels were correlated with T2D or obesity.

Design and methods: Out of 1653 individuals aged 55 to 74 years participating in the population-based KORA Survey S4 (KORA/Cooperative Health Research in the Region of Augsburg) in Southern Germany, 236 patients with T2D, 242 subjects with impaired glucose tolerance and 244 normoglycaemic controls matched for age and sex were analysed for circulating MCP-1 concentrations.

Results: MCP-1 serum concentrations were not associated with impaired glucose tolerance, type 2 diabetes or several parameters of obesity. Moreover, systemic MCP-1 levels were not significantly correlated with all but one (fasting triglycerides) of the biochemical markers tested.

Conclusions: Our data indicate that MCP-1 levels are not associated with T2D and that the contribution of fat mass to systemic MCP-1 protein might be low, suggesting that the possible local pathogenic role of MCP-1 may not be reflected by increased systemic levels of MCP-1.

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