The prevalence of type 2 diabetes (T2D) is increasing dramatically and T2D has become one of the major global health threats. Intensive research over the last decade has shown that ectopic lipid storage outside the adipose tissue, particularly in the liver and skeletal muscle, actively contributes to the development of insulin resistance, which in turn leads to T2D. Understanding the molecular mechanisms that control the storage of ectopic fat is therefore of paramount importance in order to find novel approaches that

effectively prevent the occurrence, as well as improve the treatment, of T2D.

Our latest research in extensive patient material, human cells and unique animal models has shown that the kinase STK25 is a new key regulator of lipid metabolism. Our studies show that STK25 binds to lipid droplets inside the liver cell and controls lipid accumulation and inflammation in the liver, and regulates the body's insulin sensitivity. Furthermore, we have identified selective and potent pharmacological inhibitors of STK25, which could potentially lead to a new unique treatment for T2D.

The aim of the project is to map the molecular mechanisms that regulate lipid storage and the development of insulin resistance in the liver, focusing on STK25. The study contributes to the understanding of the complex and integrated signaling pathways that regulate insulin sensitivity and the changes that lead to T2D. The project may also form the basis for the development of new treatments for T2D and related metabolic diseases, based on pharmacological inhibitors of STK25.