Beta Cell Defects

Insulin production and secretion by pancreatic beta cells is essential for human life but altered in metabolic diseases such as type 2 diabetes. During the pathogenesis of type 2 diabetes, at least two different pathological events are involved: reduced insulin secretion by beta cells in relation to ambient blood glucose levels as well as a reduction in beta cell numbers due to beta cell death (apoptosis) or dedifferentiation. Previous studies demonstrated that several stress-associated signaling pathways involving both non-coding RNAs and proteins negatively affect insulin secretion and beta cell numbers. Several extracellular (inflammation, glucolipotoxicity) and cell autonomous (oxidative stress, ER stress, DNA damage) mediators are thought to underlie activation of these evolutionarily conserved stress signaling pathways in diabetes.

The focus of the junior research group is on defining and clarifying these pathological processes and signaling pathways on the molecular level.

The junior research group studies evolutionarily conserved, cellular stress-associated non-coding RNAs (such as microRNAs) and proteins in vitro, in and ex vivo. We examine functional alterations and interactions on the level of single proteins (i.e. post-translational modifications), the cell (i.e. transcriptome), and the whole organism (i.e. role of circulating hormones) using tools and methods from biochemistry, molecular biology, genetics and physiology. The junior research group is especially interested in defining and characterizing novel regulators of apoptosis involved in type 2 diabetes-associated beta cell dysfunction and loss.

Selected Publications