GABA signaling: A route to new pancreatic β cells

Abstract

An ability to convert between pancreatic islet cell types may provide a new approach to replace insulin-secreting β cells destroyed by autoimmune attack in Type 1 diabetes. Two papers, which have recently appeared in Cell, describe how this might be achieved.

Figure 1

Mechanisms through which GABA receptor agonists or artemisinins may be used to provoke an α to β cell fate switch to correct the destruction of β cells in T1 DM. Clockwise from top left: β cells (green) are destroyed in T1 DM, leaving α cells (red) largely unaffected. Artemisinins prompt the upregulation of GABA_A receptors (orange), favoring the actions of GABA to prompt the conversion of a proportion of α cells to an intermediate phenotype (yellow). Further proliferation and redifferentiation replenishes the depleted β cell pool, restoring normal glycemia.