I am interested in how changes in cellular energy metabolism contribute to the development and progression of metabolic diseases including diabetes. Identifying changes of mitochondrial function in different stages of obesity or diabetes may reveal new targets for treatment and prevention.
Blood cell bioenergetics as a marker for metabolic health
Peripheral blood mononuclear cells (PBMCs) are an easily accessible cell population that has been shown to report systemic metabolic changes and diseases in a number of studies. As part of the RESET study (maybe a link here to the study on the homepage, I´ll ask Dorthe about it) I am testing whether mitochondrial respiration and glycolytic capacity of PBMCs reflect the metabolic health of individuals with a high risk of developing type 2 diabetes (T2D).
Type 1 diabetes (T1D) candidate genes and mitochondrial function in cytokine-induced beta cell death
Pancreatic beta cells have a very characteristic cellular metabolism, which allows them to perform their biological function of glucose-stimulated insulin secretion. Genes that are associated with the risk of T1D have been implied in mediating or protecting against cytokine-induced beta cell dysfunction and I am investigating in different cell models whether this occurs on the level of mitochondrial function.
Blood cell bioenergetics in individuals with high risk of developing T2D, undergoing 13 weeks of time-restricted eating
Aim: To examine if a 13-week time-restricted eating intervention changes blood cell bioenergetics in individuals with a high risk of developing T2D. To test if changes in cellular metabolism reflect systemic effects or explain part of the systemic phenotype.
Collaborators: K. Færch, J. Salling Quist
Cytokine effects on pancreatic beta cell bioenergetics and the modulation by T1D candidate genes
Aim: To test the effect of T1D candidate genes on beta cell bioenergetics by assessing cytokine-induced beta cell damage in overexpression and knockdown models.