Daniel Espes

The destruction and proliferation of beta cells

Type 1 diabetes is the most common chronic disease among children and adolescents and due to the long-term complications associated with the disease it decreases life-expectancy by more than 10 years. Type 1 diabetes develops due to progressive loss of the insulin producing beta-cells following an immune attack. However, the underlying trigger for the immune system is still unknown. At onset of hyperglycemia 60-70% of the beta-cell mass have already been lost, based on autopsy studies. Currently there are no clinically validated techniques for evaluating beta-cell mass in vivo and hence our understanding of how beta-cell mass is altered in health and disease is limited to what we have learned based on autopsy studies. By using radioactively labeled positron emission tomography (PET) tracers specific for beta-cells it would be possible to determine the beta-cell mass in vivo. PET is a highly sensitive, quantitative and non-observer dependent medical imaging technique in which radiolabeled molecules are used for tracking biological processes and receptors. My group is focused on the development of novel clinically applicable techniques for assessing beta-call mass and methods that non-invasively can image and quantify the immune response within the human pancreas during the development of diabetes.

We also aim to identify mechanisms involved in beta-cell destruction and novel drugs/substances with the potential to increase the proliferation of beta-cells in order to establish regenerative therapies for type 1 diabetes. For that purpose, we apply both experimental in vitro and in vivo techniques in order to study beta-cell physiology.

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