The role of the c-Jun N-terminal kinase (JNK) pathway in insulin resistance

Abstract

Obesity is usually associated with a decreased response to insulin, a major metabolic defect known as insulin resistance and an early trait in the development of type 2 diabetes. The c-Jun N-terminal kinase (JNK) pathway has emerged as a central regulator of insulin sensitivity, locally and systemically, thereby, of body’s metabolic homeostasis. As the incidence of obesity and type 2 diabetes has alarmingly increased in the last few decades, there is a tremendous necessity to identify novel pharmacological targets to efficiently improve the therapeutic outcome. In this regard, the JNK pathway seems to meet most of the requirements for being an adequate candidate to direct pharmacological intervention.