[Chemerin induces insulin resistance in C2C12 cells through nuclear factor-κB pathway-mediated inflammatory reaction]

To explore the insulin resistance-inducing effect of chemerin on murine C2C12 myoblasts and the underlying molecular mechanism.

Following 24-hour treatment with various concentrations of chemerin (0, 10, 100) ng/mL and 30-minute insulin stimulation in C2C12 cells, the glucose uptake was evaluated using a fluorescence microplate reader. ELISA was used to detect the levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor α (TNF-α) in culture fluid. In addition, the expression of nuclear factor κB (NF-κB) was determined by Western blotting. The underlying mechanism involved in chemerin-induced insulin resistance was evaluated with the precondition of NF-κB blocker pyrrolidine dithiocarbamate (PDTC).

Chemerin inhibited the glucose uptake of C2C12 cells in a dose-dependent manner, concomitant with the increases of IL-6, IL-8, TNF-α levels. Furthermore, chemerin stimulation improved the expression of NF-κB. However, pretreatment with NF-κB blocker PDTC significantly abated the inhibitory effect of chemerin on glucose uptake, and also obviously decreased the levels of IL-6, IL-8 and TNF-α induced by chemerin.

Chemerin might induce insulin resistance in C2C12 cells through NF-κB pathway-mediated inflammatory reaction.