Abstract
The natural history of type 2 diabetes is characterised by worsening hyperglycaemia and progressive deterioration in function of the insulin-secreting pancreatic β cells.1 Despite intense investigative efforts, the pathophysiological basis underlying β-cell dysfunction (and the concomitant loss of β-cell mass) remains unclear. Nevertheless, the central importance of declining β-cell function in type 2 diabetes is underscored by its correlation with a progressive loss of glycaemic control, which typically occurs over time.
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