The interaction between adipokines, diet and exercise on muscle insulin sensitivity

Purpose of review High-fat diets lead to obesity and increase the risk of developing insulin resistance and type 2 diabetes. Adipose tissue and skeletal muscle act as endocrine organs, and produce various cytokines that can potentially alter peripheral insulin sensitivity. The purpose of the present review is to briefly summarize the effects of major cytokines (leptin, adiponectin, tumor necrosis factor-a, and interleukin-6) on muscle metabolism and insulin response, with a focus on the effects of diet and exercise. Recent findings Leptin and adiponectin improve insulin sensitivity. However, in obesity there is a diminished response to these adipokines. This resistance can be induced very rapidly and may lead to subsequent impairments in insulin response. Tumor necrosis factor-a is a proinflammatory cytokine that has been implicated as a mediator of insulin resistance, particularly in obesity. Interleukin-6 was the first identified myokine. There is evidence to implicate interleukin-6 both as a mediator of impaired insulin action in obesity, and also as a facilitator of increased fuel metabolism during exercise. The effect of each of these cytokines on muscle insulin sensitivity can be modulated by diet and exercise. Summary Much of the information summarized in the present review focuses on the effects of various cytokines in isolation, although in vivo there can be considerable interaction with each other. Future research should consider these potential interactions.