aurapten and Insulin-Resistance

Inflammation plays a key role in obesity-related pathologies such as insulin resistance and type 2 diabetes. Hypertrophied adipocytes trigger the enhancement of macrophage infiltration and the release of various proinflammatory factors in obese adipose tissue. In this study, we examined whether auraptene, a citrus-fruit-derived compound, could suppress the production of inflammatory factors that mediate the interaction between adipocytes and macrophages.. Experiments using a co-culture system of 3T3-L1 adipocytes and RAW264 macrophages showed that auraptene reduced the production of nitric oxide and tumor necrosis factor-α. In RAW264 macrophages, auraptene also suppressed the inflammation induced by either LPS or the conditioned medium derived from 3T3-L1 adipocytes. In addition, auraptene inhibited the phosphorylation of the p38 mitogen-activated protein kinase and suppressed the production of proinflammatory mediators in activated macrophages.. Our findings indicate that auraptene exhibits anti-inflammatory properties by suppressing the production of inflammatory factors that mediate the interaction between adipocytes and macrophages, suggesting that auraptene is a valuable food-derived compound with a potential to attenuate chronic inflammation in adipose tissue and to improve obesity-related insulin resistance.

Topics: 3T3-L1 Cells; Adipocytes; Adipose Tissue; Animals; Anti-Inflammatory Agents; Cell Line, Tumor; Chemokine CCL2; Citrus; Coculture Techniques; Coumarins; Culture Media, Conditioned; Fruit; Inflammation; Insulin Resistance; Lipopolysaccharides; Macrophages; Mice; Nitric Oxide; Obesity; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Plant Extracts; Tumor Necrosis Factor-alpha