Role of protein SUMOylation in glucose homeostasis and type 2 diabetes

Type 2 diabetes is a significant public health issue and its prevalence is rapidly increasing. It is thought to be caused by hepatic and peripheral insulin resistance, as well as deficiencies in beta-cell insulin secretion, but exactly how these processes become defective is still unclear. SUMOylation is a post-translational modification, analogous to ubiquitination. It has many nuclear roles, and it is also involved in neurotransmitter-receptor trafficking and neurotransmitter release. These processes have striking similarities with the intracellular pathways for insulin release and insulin responsiveness. Several studies have shown that insulin release is affected by SUMOylation, and that it might be defective in patients with advanced type 2 diabetes.

My hypothesis is that protein SUMOylation plays a key role in glucose homeostasis and the pathology of type 2 diabetes. The key goals of this project are to establish the mechanism for control of insulin release by SUMOylation and identify new SUMOylation substrates involved in diabetes and glucose homeostasis.

The findings of this study will open new avenues in research into type 2 diabetes and has the potential to identify novel therapeutic targets for the disease.