Cell therapy for type 2 diabetes: Is it desirable and can we get it?

Abstract

The functional mass of β-cells is decreased in type 2 diabetes. Replacing missing β-cells or triggering their regeneration may thus allow for improved treatment of type 2 diabetes, to the extent that this is combined with therapy for improved insulin sensitivity. Although progress has been made in deriving β-cell-like cells from stem or precursor cells in vitro, these cannot yet be obtained in sufficient quantities or well enough differentiated to envisage their therapeutic use in β-cell replacement therapy. Likewise, our very limited understanding of β-cell regeneration in adult man does not yet allow for development of a valid strategy for kick-starting such a process in individuals with type 2 diabetes, whether by bona fide neogenesis or self-replication of existing β-cells. Regardless of how β-cell mass is restored in type 2 diabetes, it will be important to prevent any renewed decrease thereafter. Current understanding suggests that islet inflammation as well as signals from (insulin-resistant/inflamed) adipose tissue and skeletal muscle contribute towards decreased β-cell mass in type 2 diabetes. It will likely be important to protect newly formed or implanted β-cells from these negative influences to ensure their long-term survival. © 2008 The Authors Journal Compilation © 2008 Blackwell Publishing Ltd.