Abstract

Recent studies in animal models and human pathological specimens suggest the involvement of β-cell dedifferentiation in β-cell dysfunction associated with type 2 diabetes. Dedifferentiated β-cells may be exploited for endogenous renewal of the β-cell mass. However, studying human β-cell dedifferentiation in diabetes presents major difficulties. We have analysed mechanisms involved in human β-cell dedifferentiation in vitro, under conditions that allow cell proliferation. Although there are important differences between the two cellular environments, β-cell dedifferentiation in the two conditions is likely to share a number of common pathways. Insights from the in vitro studies may lead to development of approaches for redifferentiation of endogenous dedifferentiated β-cells.

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