Endocrine Abstracts

A decrease in the number of functional insulin producing beta-cells contributes to the pathophysiology of type 2 diabetes. The putative factors responsible for the maladaptation of beta-cells include hyperglycaemia, cytokines, dyslipidemia and leptin. Islet inflammation, autoimmunity and some drugs may be secondary modulators. Predetermined amount of beta-cell mass, sensitivity to pro-apoptotic signals and regeneration potential of beta-cells are predisposing factors. The mechanisms regulating β-cell proliferation and apoptosis share common pathways with those responsible for the regulation of β-cell function and are therefore inseparable processes. Understanding that decreased β-cell mass is an important factor in the pathogenesis of type 2 diabetes, raises a concern regarding the application of drugs potentially harming the remaining β-cells. Conversely, protection of the β-cells appears as a new therapeutic target not only for type 1 but also for type 2 diabetes.