Currently, there is no curative therapy for diabetes, which can restore survival and function of the insulin producing beta-cells.

The research of my group focuses on the understanding of the mechanisms of the decreased beta cell survival, what signals make the β-cell proliferate and survive or die. We develop targets to maintain normoglycemia and beta-cell survival and test these in vitro and in preclinical models of diabetes.

In type 2 diabetes, there is a defect in the peripheral insulin sensitivity (insulin resistance) as well as in the insulin producing pancreatic beta cell. A decrease in the number of functional insulin producing β-cells together with an intrinsic defect in the secretory machinery contributes to the pathophysiology of type 2 diabetes.

We observed that β-cell death in type 2 diabetes is triggered by an inflammatory attack, very reminiscent to type 1 diabetes, and this links both diseases.

Recent results from our group on human pancreatic islets will be implicated into the clinic, that the focus of both types of diabetes is to rescue the β-cell. We have described the mechanisms of glucose induced apoptosis on pancreatic β-cells and suggested a specific therapy for diabetes, namely the Interleukin-1 Receptor antagonist, which we showed to be able to protect from glucotoxicity and apoptosis in vitro. Large clinical studies have proven our inital results from pancreatic islets.

One model in our lab is obesity. Here, we can learn, how the β-cell compensates for the increased insulin demand in the face of insulin resistance by increasing its functional mass. In diabetes, such compensatory mechanisms are lost, and apoptosis occurs. We aim to find pathways which switch apoptotic signalling into proliferation and targets to protect the β-cell from an inflammatory attack to maintain a functional β-cell mass.