The Institute

Impairment and/or loss of pancreatic islet beta cells are at the origin of all forms of diabetes, leading to increased blood glucose levels. Scientists of the IPI/PLID are working to decipher the causal mechanisms for these deficiencies with the aim of developing new approaches to protect or restore beta cell function and viability.

Specifically, we are investigating the molecular basis for the production, storage and secretion of insulin secretory granules, in which beta cells store insulin, as well as the lipid composition of the beta cell plasma membrane to understand how modifications in its composition, e.g. following insulin secretory granule exocytosis, affect signaling properties of membrane receptors. We are also defining the genetic, epigenetic and physiological traits of human islets from metabolically phenotyped non-diabetic, prediabetic and diabetic subjects to understand molecular changes associated with beta and alpha cell dysfunction along the natural history of type 2 diabetes. Integration of these data with medical records and clinical chemistry laboratory data shall enable the identitification of reliable biochemical biomarkers for progression towards type 2 diabetes in stratified groups of subjects. Moreover, the IPI/PLID support physicians who participate in multicenter clinical trials of the German Center for Diabetes Research for prevention and therapy of type 2 and gestational diabetes.

IPI/PLID investigators are also working on the development of therapies to replace or regenerate damaged or destroyed beta cells by exploiting regeneration models in mice and zebrafish. Strong effort is placed on auto- and allogeneic transplantation of pancreatic islets from human organ donors for the therapy of type 1 diabetes. Toward this aim, we are developing in parallel protocols for xenotransplantion of porcine islets and the transplanation of human induced pluripotent stem cell-derived beta cells in next generation encapsulation devices.

Key aims of the IPI/PLID are the identification of biomarkers for early identification of subjects with high risk of developing type 1 diabetes as well the immunoprevention of this disease through the induction of antigen-specific immunotolerance towards beta cells.

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