Insulin plays a crucial role in regulating the proper metabolic and energy balance. Once insulin signal transmissions are decreased, this can lead to a condition known as insulin resistance.
Difference mediators, such as pro-inflammatory cytokines, free fatty acids, blood glucose and ROS level can increase the activity of kinases, i.e. several Protein kinase C (PKC) isoforms, c-Jun N-terminal kinases (JNK), Protein kinase A (PKA), Mammalian Target of Rapamycin (mTOR) and Mitogen-Activated Protein Kinase (MAPK), which affecting the signal of insulin receptors, IRS, and downstream-located effector molecules. Therefore, better understanding on the molecular mechanisms of these pathways is important for developing a more effective treatment of insulin resistance and associated diseases.
This review summarizes the current knowledge on the mechanism of insulin resistance, the diseases associated with insulin resistance and biological effects of recent agents, which are developed for increasing insulin signaling, and are currently undergoing clinical trials.