Activation of invariant natural killer T cells by lipid excess promotes tissue inflammation, insulin resistance, and hepatic steatosis in obese mice

摘要: Obesity triggers a low-grade systemic inflammation, which plays an important role in the development of obesity-associated metabolic diseases. In searching for links between lipid accumulation and chronic we examined invariant natural killer T (iNKT) cells, subset lymphocytes that react with lipids regulate inflammatory responses. We show iNKT cells respond to dietary excess become activated before or at time tissue recruitment leukocytes, these progressively increase proinflammatory cytokine production obese mice. Such skew other leukocytes toward induce imbalanced environment multiple tissues. Further, cell deficiency ameliorates inflammation provides protection against obesity-induced insulin resistance hepatic steatosis. Conversely, stimulation using canonical agonist exacerbates disease. These findings place into complex network linking obesity suggest new therapeutic avenues disorders.