Understanding how beta-cells maintain themselves in the adult pancreas is important for the development of strategies aimed at ameliorating or ideally curing different forms of diabetes. There has been much debate over whether beta-cell proliferation, as a means of self-renewal, predominates compared to the existence and differentiation of a pancreatic stem cell or progenitor cell population. Based on studies in the mouse, both principles can be demonstrated, although in normal physiological conditions beta-cell proliferation is the dominant mechanism. However, it is not clear how well these rodent studies can be extrapolated to human physiology. Beta-cell proliferation is extremely limited in human and there are several lines of evidence suggesting that islet neogenesis may be more prominent mechanism in the human than in the rodent pancreas. The plasticity of human beta cells may be greater than expected. However, induction of beta-cell differentiation in vitro remains a major challenge. Our recent observations on the physiological microenvironment of human islets may provide keys to solve this problem.
03 - 07 May 2008
European Society of Endocrinology