Profile of the Junior Research Group

Of all human organs, the skeletal muscle is the largest glucose-storage organ. Skeletal muscle contributes on average 38 percent and 31 percent to male and female body mass and skeletal muscle stores 300-500 grams of glucose in the form of glycogen. In comparison, the adult liver stores about 100-120 grams of glycogen. Skeletal muscle is a key organ in postprandial glucose disposal and insulin-resistant muscle which takes up and stores considerable less glucose per unit of insulin is a key risk factor for developing type 2 diabetes.

During exercise, skeletal muscle efficiently extracts glucose from the circulation. This exercised-induced glucose uptake involves molecular signaling steps that are distinct from those activated by insulin (Sylow et al., 2017). Exercised-stimulated glucose uptake is preserved in skeletal muscle from humans with insulin resistance and diabetes (Kennedy et al., 1999), highlighting a key reason why exercise is considered a therapeutic cornerstone for patients with type 2 diabetes (Colberg et al., 2010). We are interested in decoding the molecular signaling pathways underpinning exercise regulation of glucose metabolism. This research could potentially identify novel therapeutic targets to treat insulin resistance and type 2 diabetes. Furthermore, we are using novel genetic tools to simultaneous activate several endogenous genes within skeletal muscle to reverse insulin resistance and type 2 diabetes.