Background/Aims: Obesity is associated with a low-grade inflammation, insulin resistance, and macrophage infiltration of adipose tissue. The role of CC chemokines and their respective receptors in human adipose tissue inflammation remains to be determined. Methods: sc and visceral adipose tissue of obese patients (body mass index 53.1 ± 11.3 kg/m²) compared with lean controls (body mass index 25.9 ± 3.8 kg/m²) was analyzed for alterations in inflammatory gene expression. Results: Macrophage infiltration was increased in sc and visceral adipose tissue of obese patients as determined by increased mRNA expression of a macrophage-specific marker (CD68) and by elevated macrophage infiltration. Gene expression of CC chemokines involved in monocyte chemotaxis (CCL2, CCL3, CCL5, CCL7, CCL8, and CCL11) and their receptors (CCR1, CCR2, CCR3, and CCR5) was higher in sc and visceral adipose tissue of obese patients. Serum concentrations of the inflammatory marker IL-6 and C-reactive protein were elevated in obese patients compared with lean controls. Obese patients revealed increased insulin resistance as assessed by the homeostasis model assessment of insulin resistance index and reduced plasma adiponectin concentrations. Adipose tissue expression of many CC chemokines and their receptors in the obese group positively correlated with CD68 expression. Conclusion: Up-regulation of the CC chemokines and their respective receptors in adipose tissue occurs in human obesity and is associated with increased systemic inflammation.

The association of obesity, insulin resistance, and chronic low-grade inflammation has been evident for several years by now. Since obesity, insulin resistance, and inflammation all are related to aging as well, the mechanisms underlying this association are of critical importance for gerontology. Although several molecular and cellular mechanisms by which inflammatory events decrease the sensitivity to insulin in obese patients have recently been elucidated, the pathogenesis of obesity-induced insulin resistance is still obscure in many aspects. This review aims at giving a general view on the known mechanisms and summarizing the recent progress. Research currently focuses on adipose tissue inflammation as predominantly driven by adipose tissue macrophages, but also related alterations in other organs (liver, muscle, pancreas) have to be considered. Moreover, novel approaches for treatment and prevention of insulin resistance and type 2 diabetes by targeting obesity-induced inflammatory processes are discussed here.

Inflammatory alterations in white adipose tissue appear to underlie complications of obesity including diabetes mellitus. Polyunsaturated fatty acids (PUFA), particularly those of the n−3 series, modulate immune responses and may ameliorate insulin sensitivity. In this study, we investigated how PUFA affect white adipose tissue inflammation and gene expression in obese diabetic animals.