Proper function of pancreatic β-cells as glucose sensors throughout life is critical for maintaining glucose homeostasis in the body. Deterioration in the function and quantity of β-cells is fundamental to the development of diabetes. The activity of β-cells is also closely related to the function of other endocrine cells in the pancreatic islets. Although insulin was discovered 100 years ago (1922) and the major signaling pathway leading to insulin secretion has since been described, we still lack many details about the mechanisms of action of pancreatic β-cells and islet cells that would help us prevent and control diabetes, one of the world's major health problems.
To improve our understanding of how diabetes develops, our lab is studying the details of glucose metabolism in β-cell signaling. We are focusing on:
1. The role of redox signaling and lipid metabolism in β-cells upon glucose stimulation under physiological and pathophysiological conditions.
2. The interplay between β-cells and other endocrine cells in pancreatic islets in response to altered redox status of β-cells.
Our research is performed in a variety of models with diverse level of complexity, ranging from cell cultures to isolated mouse pancreatic islets to whole animals (mice). We use novel experimental strategies in combination with modern omics analyzes.
Fluorescent insulin injected into a mouse pancreatic islet:
Biphasic insulin release (left) after glucose stimulation of islets from mice fed a normal vs. high-fat diet and the corresponding glucose levels (right).
Mouse pancreatic islets surrounded by exocrine tissue, nuclei (blue), Cre recombinase activity in beta cells (blue), beta cells without Cre recombinase aktivity (pink).
Mouse pancreatic islet, by hematoxylin and eosin staining, nuclei (blue), insulin (pink), glucagon (brown).
