Irisin Reverses Insulin Resistance In C2C12 Cells Via The P38-MAPK-PGC-1? Pathway

ObjectiveInsulin resistance(IR)is a fundamental pathogenic factor shared by a myriad of metabolic disorders,especially in type 2 diabetes.The mechanism of IR is usually accompanied by mitochondrial dysfunction.Irisin has been proposed to act as a hormone in the regulation of energy homeostasis and metabolism.Our research expects to investigate the effect of irisin on IR and further ameliorating metabolism disease.Materials and MethodsWe induced IR in C2C12 myotube cells by making them expose to 100 n M insulin for 24-48 h.Technology such as Western blot and RT-PCR were used to determine the effect of irisin mediated alterations in insulin related signaling as well as glucose uptake ability in IR C2C12 cells.Extracellular acidification rate(ECAR)and oxygen consumption rate(OCR)were assessed with seahorse system to investigate the effects of irisin on mitochondrial metabolism.And SPSS 20.0 statistical software were performed to analyze the result.ResultsOur research demonstrates that irisin can partially restore the glucose uptake capacity mainly through the p38 MAPK pathway and stimulate the expression of mitochondrial genes in IR C2C12 cells.Moreover,irisin can inhibit mitochondrial glycolysis of IR C2C12 cells and stimulate their respiration ability.Thus,there may have the therapeutic potential of irisin on insulin resistance through p38-MAPK-PGC-1? pathway.ConclusionOur research found irisin improve glucose uptake through the p38 MAPK/PGC-1? axis in IR C2C12 cells,which will be meaningful in the type 2 diabetic patients.