Tissue Embelin inflammation is now recognized as a major cause of impaired insulin sensitivity in obesity and has been Ceftizoxime sodium observed in all classical insulin target tissues including fat, liver and muscle. Interleukin 1 Beta is an important proinflammatory cytokine that binds to the type 1 IL-1 Receptor and has well described proinflammatory effects. Signal transduction is elicited by interaction of the IL1R1 with an accessory protein. The endogenous antagonist IL-1R Antagonist, also binds to the IL-1R1 but does not initiate signal transduction. IL-1Ra is classically viewed as an anti-inflammatory cytokine that acts as a selective, competitive receptor antagonist at the IL-1R1 by blocking the actions of IL-1b and the balance in expression between IL-1b and IL-1Ra is important in many inflammatory diseases. While the anti-inflammatory role of IL-1Ra in the pancreas is well established in both mice and humans, the role of IL-1Ra in other insulin target tissues and the general role of systemic levels of IL-1Ra in the development of obesity and insulin resistance is still unclear. A number of studies over the last decade have raised the question of whether the high levels of IL-1Ra observed in obesity may contribute to the development of insulin resistance. In obese human patients, circulating levels of IL-1Ra are,6.5 times higher than lean subjects and, interestingly, the levels of IL-1Ra in plasma correlate more closely with insulin resistance than BMI, suggesting an important link between IL-1Ra and insulin resistance. Indeed, elevated systemic concentrations of IL-1Ra are associated with an increased risk of developing type 2 diabetes, and in retrospective studies this increase in IL-1Ra accelerated prior to type 2 diabetes diagnosis. In a recent study IL-1Ra was even identified as a novel biomarker for clinically incident diabetes, over and above the classical risk factors such as BMI and waist: hip ratio. Supporting a possible role in the development of insulin resistance, thiazolidinedione treatment significantly reduced levels of IL-1Ra in patients with metabolic syndrome, as well as in cell culture studies where TZDs inhibited the production of IL-1Ra from proinflammatory adipocytes.