The AMP-activated protein kinase (AMPK) is a highly conserved and ubiquitously expressed protein,  sensesing and regulating cellular energy levels. Its activation by existing and candidate diabetic drugs forms a mechanistic basic for the treatment of type 2 diabetes (T2D) due to predicted beneficial effects in liver and muscle tissue. Thus, pharmacological activation of AMPK is a suggested and intensely studied strategy for the treatment of insulin resistance and diabetes. The effect of AMPK activation in adipose tissue however remains poorly understood.

The inability of subcutaneous tissue to adequately store excess energy is a major underlying cause of insulin resistance and type 2 diabetes (T2D). Due to its ability to inhibit lipolysis and stimulate glucose uptake and fatty acid (FA) synthesis (lipogenesis), insulin is known as the most important regulator of lipid storage. The exact mechanisms for how insulin stimulates FA synthesis are not known however, presvious results suggest an involvement of insulin-induced AMPK inhibition.

The overall aim of my research is to investigate the effects AMPK activation has on adipocyte metabolism and characterize the effect insulin has on AMPK activity and the underlying mechanism.