Interleukin-1beta induces the novel adipokine chemerin in adipocytes in vitro

Chemerin has recently been characterized as a novel adipokine playing a crucial role in adipocyte differentiation and insulin signalling. In the current study, the impact of insulin resistance-inducing and proinflammatory interleukin (IL)-1beta on chemerin protein secretion and mRNA expression was determined in 3T3-L1 adipocytes. Interestingly, IL-1beta significantly induced chemerin protein secretion almost 1.3-fold from 5.89 ng/ml (basal) to 7.52 ng/ml. Furthermore, chemerin mRNA synthesis was significantly stimulated by IL-1beta in a dose-dependent fashion with 1.5-fold induction seen at IL-1beta concentrations as low as 0.07 ng/ml and maximal 2.6-fold upregulation found at 2 ng/ml effector. Induction of chemerin mRNA by IL-1beta was time-dependent in both 3T3-L1 adipocytes and brown fat cells. Signalling studies suggested that Janus kinase 2, nuclear factor kappa B, p44/42 mitogen-activated protein kinase, and phosphatidylinositol 3-kinase are involved in IL-1beta-induced chemerin mRNA expression. Furthermore, recombinant chemerin downregulated insulin-stimulated glucose uptake. Taken together, we show that chemerin is upregulated in fat cells by IL-1beta and might modulate the effects of IL-1beta on adipocyte metabolism and insulin sensitivity.