Beta cells are the guardians of glucose homeostasis in the body, and their deficiency and impaired function trigger the development of diabetes. We focus on the role of redox homeostasis and lipid metabolism during glucose stimulation and subsequent signaling in beta cells. Altered redox status and modified glucose-induced lipid metabolism may affect cellular signaling i.e. insulin secretion, while in the long term they may induce cellular stress. The switching point and metabolic targets of signaling are unknown in beta cells. The aim of this PhD project is to identify redox regulated glucose-induced lipid signaling and lipid metabolism under physiological conditions of insulin secretion on the one hand and the mechanism of its dysregulation to develop diabetes on the other hand. A unique mouse model with altered redox status in beta cells and isolated Langerhans islets/cells will be used for the study, employing novel experimental strategies in combination with omics analyses.