The pancreatic β-cell: birth, life and death

Defective insulin secretion is a hallmark of all forms of diabetes. Whereas Type 1 diabetes has long been known to result from the immune-mediated destruction of β-cells, Type 2 diabetes appears to involve both loss of β-cell mass and glucose sensitivity in the face of extrapancreatic insulin resistance. We summarize here the proceedings of a Biochemical Society Focused Meeting, held at the St Thomas campus of King’s College London in December 2007, which highlighted recent research advances targeting the β-cell. Introduction It has become increasingly clear in the last few years that pancreatic β-cell failure or destruction lies at the heart not only of Type 1, but also of Type 2 diabetes. Although these two diseases have strikingly distinct aetiology (Type 1 is an early-onset autoimmune disease involving β-cell destruction [1], whereas Type 2 diabetes is seen later in life and usually involves both insulin resistance and β-cell failure and/or loss [2]) the ability to protect, rejuvenate or reintroduce β-cells into patients with either form has recently become a focus of vigorous research. Importantly, and as discussed by Philippe Froguel (Imperial College) at the meeting, whole-genome association studies for Type 2 diabetes [4–7] have implicated a new set of genes which, unexpectedly, all appear to be involved in β-cell function and/or development. The recent demonstration of the feasibility of generating pluripotent stem cells from the skin cells of non-human primates [8], and thus a genuine chance ultimately to obtain new β-cells, have emphasized the importance of achieving a deeper understanding of the ‘life cycle’ of these remarkable cells.