Beta cells in type 2 diabetes – a crucial contribution to pathogenesis

The healthy beta-cell has an enormous capacity to adapt to conditions of higher insulin demand (e.g. in obesity, pregnancy, cortisol excess) to maintain normoglycaemia with an increase in its functional beta-cell mass. This compensates in 80-90% of individuals for insulin resistance. However, in 10-20% of individuals, the beta-cells are unable to match the demands of insulin resistance and insulin levels are relatively insufficient to maintain normal glycaemic control. This eventually leads to glucose intolerance and type 2 diabetes (T2DM). Accordingly, preservation of functional beta-cell mass has become central in the treatment of type 1 diabetes as well as T2DM. The purpose of this review is to summarize the recently described mechanisms of beta-cell death in T2DM and to postulate possible new targets for treatment.