Can we make a better beta cell?

Excerpt

The International Diabetes Federation has recently announced that 415 million people worldwide currently have diabetes, and this incidence is predicted to increase to 642 million by 2040 [1]. It has long been recognised that beta cell destruction underpins type 1 diabetes, but it has become apparent only relatively recently that individuals with long-term type 1 diabetes still show residual beta cell turnover [2]. Reductions in beta cell mass are also involved in the aetiology of type 2 diabetes [3], so devising strategies for preserving a functional mass of beta cells to maintain normoglycaemia in people with both type 1 and type 2 diabetes is a fast moving area of research. The availability of unlimited numbers of beta cells derived from human embryonic stem cells or induced pluripotent stem cells is becoming a realistic therapeutic strategy, with recent studies providing robust protocols for the generation of billions of human beta-like cells without genetic modification [4, 5]. However, beta cell replenishment in situ is also a possibility and the EASD/JDRF symposium on ‘Can we make a better beta cell?’ at the 51st EASD annual meeting in Stockholm in September 2015 aimed to disseminate approaches distinct from the use of exogenously generated beta cell substitutes. The presentations addressed strategies for promoting beta cell mass expansion through transdifferentiation, regeneration and repair in situ, and mechanisms regulating the differentiated function and survival of endogenous beta cells in the normal pancreas, with the aim of identifying novel targets for therapeutic intervention. Three thought-provoking lectures were delivered during the symposium, each of which generated wide-reaching questions and discussion. …