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ULB Center for Diabetes Research
Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycemia that can lead to chronic complications such as cardiovascular disease, blindness and kidney failure. Loss of functional β-cell mass is the key mechanism leading to the two main forms of diabetes mellitus, type 1 and type 2 diabetes. In order to prevent or revert diabetes, it is critical to understand the mechanisms behind β-cell failure, and this is one of the main objectives of the UCDR. There are basic pathogenic differences in the two forms of diabetes, i.e. immune-mediated in type 1 diabetes and metabolic in type 2 diabetes, which differentially impact early β-cell dysfunction and eventual fate.
In recent years there have been major advances in the field, mostly delivered by studies on β-cells in human disease. These include studies of islet morphology and human β-cell gene expression in type 1 and type 2 diabetes, the identification and characterization of the role of diabetes candidate genes at the β-cell level, and endoplasmic reticulum stress signaling that contributes to β-cell failure in both forms of diabetes. Current therapies consist of insulin administration or drugs that increase insulin secretion or insulin sensitivity, but unfortunately none of them prevent the progressive loss of functional β-cell mass. Thus, research to develop novel treatment strategies to protect pancreatic β-cells in diabetes is urgently needed.
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