Abstract
Insulin resistance (IR) is a fundamental pathogenic factor shared by a myriad of metabolic disorders, including obesity and 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. However, the effects of irisin on IR and mitochondrial function have not yet been fully investigated. Here, our research shows that irisin increases glucose uptake in C2C12 myoblast cells via the p38-mitogen-activated protein kinase (MAPK)-PGC-1α pathway. Irisin can also enhance mitochondrial function and mitochondrial respiration. Moreover, irisin stimulates autophagy via PGC-1α. Collectively, these data provide basic evidence to support the therapeutic potential of irisin for IR, which may rely on p38-MAPK-PGC-1α pathway activation and enhance mitochondrial function.