According to current figures, one in ten adults has diabetes and an equally large number has the precursor to it, prediabetes. Diabetes is the leading cause of blindness, chronic kidney failure, heart attack, stroke and leg amputations. These diabetic complications often determine the mortality of patients with diabetes. Diabetic complications are evident in subtypes of diabetes as early as the manifestation of the disease itself. However, no therapeutic approaches are currently available that specifically target intracellular metabolic pathways underlying the development of diabetic complications. In addition, it is still not possible to reliably determine the risk of late onset diabetes or to induce remission of established late complications.

The SFB1118 aims to understand diabetes complications by studying the intracellular effects of reactive metabolites (RM), such as reactive oxygen species (ROS), dicarbonyls (DC), or glucose metabolites (O-Glc-NAc), which are generated during energy metabolism.

Our previous work identified novel molecular pathomechanisms of diabetic complications as well as specific targets of RM in the development of insulin resistance, retinopathy, sensory and autonomic neuropathy, nephropathy, and diabetic cardiopathy.

Paradigm-shifting findings of this SFB demonstrated that synergistic enzyme systems and autoregulatory feedback loops determine the accumulation of RM. RM induce post-translational modifications of proteins and DNA with functional changes that are followed by cellular compensatory mechanisms, insulin resistance, DNA damage and/or senescence and can lead to tissue fibrosis and organ failure (multiple-hit concept).
The overall goal is to achieve long-term targets for prevention and remission of existing late complications in diabetes.