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Project

The role of iron metabolism in beta cell differentiation, maturation, and function. (FWOTM1035)

Diabetes is a pandemic disorder characterized by chronic hyperglycemia as a result of insulin insufficiency. Insulin is a hormone produced by the beta cells of the pancreatic islets. Current diabetes therapy strives for glycemic control but fails to solve the underlying beta cell defect. Although this approach has increased the life expectancy and quality of most patients it has turned diabetes into a chronic disease. Curative strategies should therefore aim at restoring and protecting the functional beta cell mass which in turn would reinstate a fine-tuned glucose homeostasis .

Such beta cell replacement therapy could either be achieved by transplantation of
(stem cell-derived) beta cells, or by endogenous beta cell repair
through regeneration. Improved understanding of beta cell
maturation is key to such novel therapeutic approaches. Dietary iron
overload is a risk factor for diabetes through its deleterious effects on
beta cell function. Since iron is necessary for cellular energy
metabolism, perturbations of iron metabolism in beta cells cause
decreased insulin secretion. Furthermore, iron homeostasis and
oxygen metabolism are intimately linked, and hypoxia causes a loss
of functional beta-cell maturity. In this project, I propose to study iron
metabolism at different developmental stages in mouse beta cells
and in adult human beta cells. The aim is to improve cell replacement
strategies for diabetes through a better understanding of the iron
metabolism in beta cells
Date:1 Oct 2020 →  Today
Keywords:Diabetes, iron, cellular maturation
Disciplines:Paediatrics, Cellular therapy, Endocrinology