AMP-activated protein kinase in adipose tissue
The inability of adipose tissue to adequately store excess energy is a major underlying cause of insulin resistance and type 2 diabetes (T2D). Insulin is the most important hormone to regulate lipid storage, yet the exact mechanisms for how insulin stimulates lipid synthesis are unknown. Activation of AMP-activated protein kinase (AMPK) forms a basis for anti-diabetic drugs, because of the beneficial effects that this is thought to have in liver and muscle. Effects of specific AMPK activation on adipocyte metabolism are however unexplored. Also, our previous data suggest that AMPK mediates some effects of insulin on lipid storage. In this project we therefore aim to investigate if and in that case how AMPK mediates insulin-induced lipid synthesis. Moreover, we will determine the effects that AMPK activation has on lipid metabolism in human adipocytes and explore whether altered AMPK function is linked to the development of insulin resistance.
|Effective start/end date||2017/04/01 → 2021/05/01|
- Olga Göransson - Protein Phosphorylation - EXODIAB: Excellence in Diabetes Research in Sweden (Supervisor)
- Franziska Kopietz - EXODIAB: Excellence in Diabetes Research in Sweden - Protein Phosphorylation (Research student)
- Maria Lindahl - EXODIAB: Excellence in Diabetes Research in Sweden - Glucose Transport and Protein Trafficking (Research engineer)
- Eva Degerman - Insulin Signal Transduction - EXODIAB: Excellence in Diabetes Research in Sweden (Assistant supervisor)