Skeletal muscle makes up 40% of total body weight and is the main site for metabolism of glucose and lipids. At rest, the breakdown of lipids is the primary source of energy, but during insulin-stimulated conditions, glucose is preferred energy source. Therefore, skeletal muscle has to be able to switch rapidly between lipid and glucose metabolism. However, in the setting of insulin resistance this ability is impaired. Due to skeletal muscle is responsible for 75% of the glucose uptake and utilization mediated by insulin, it has become a promising target for T2D medication.
Beta adrenergic receptor agonists have previously shown to increase glucose uptake and fatty acid oxidation in skeletal muscle cells. Activation of these receptors have also shown to contribute to muscle growth and mitochondrial biogenesis. These properties have made them promising targets for the development of new type 2 diabetes drugs. My PhD project is a collaboration with AstraZeneca in Mölndaln (Sweden) where the overall goal is to investigate the possibilities of using β-AR agonists as a treatment option in T2D focusing on skeletal muscle.