Diabetes is a severe metabolic disorder characterized by hyperglycemia due to defects in
insulin secretion and/or insulin action. Over the past decades, a continuous rise of the incidence of
diabetes is observed, leading to epidemic dimensions of the disease in large parts of the western world.
Depending on the type of diabetes, (auto-)immune processes (type 1 diabetes) or metabolic disorders
(type 2 diabetes) dominate the pathogenesis of the disease. Therefore, investigations aiming at the
identification of disease mechanisms and the development of preventive and therapeutic approaches,
focus on the identification of common regulators of both immunologic and metabolic pathways
involved in the pathogenesis of diabetes. So far, extensive research, employing clinical and
experimental approaches demonstrate a central role of heat shock proteins (HSPs) in diabetes
development. In type 1 diabetes intracellular HSPs located in the beta cell can provide efficient
protection against the deleterious effects of autoimmune effector mechanisms whereas extracellular
HSPs can stimulate the release of beta cell damaging mediators from innate immune cells or even
contribute to the induction of immune reactivity against beta cell specific antigens. In type 2 diabetes
HSPs are involved in the control of various immunologic and metabolic processes contributing to the
induction and maintenance of low-grade, subclinical inflammation associated with the development of
diabetes and related disorders such obesity and insulin resistance. The results of current research on the
pathogenesis of diabetes point to HSPs and HSP-dependent immunologic and metabolic pathways as
promising targets for strategies to prevent or cure diabetes and its sequelae.
Keywords: Heat shock proteins, type 1 diabetes, type 2 diabetes, pancreatic beta cells, adipocytes, inflammation,
autoimmunity, insulin resistance.
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