ZnT8 plays a critical role in glucose-stimulated insulin secretion

It is thought that more than a million Britons have undiagnosed type 2 diabetes mellitus, according to recent data. type 2 diabetes results from a failure of cells to use insulin properly. This β-cell dysfunction may occur due to decreased expression of zinc transporters. Zinc enables insulin storage at high concentrations and for it to be released with an increase in glucose levels. Zn homeostasis is thus very important for correct β-cell function.

El Muayed et al. treated MIN6 cells with inflammatory cytokines which altered the expression of several Zn transporters, notably ZnT8 which is needed to traffic Zn across cell and vesicular membranes. The study also showed that decreasing the expression of ZnT8 using ZnT8 siRNA in murine islet cells prevents β-cells from accumulating Zn in secretory vesicles, resulting in a reduction in labile Zn and decreased glucose-stimulated insulin secretion in cells.

These results indicate that ZnT8 expression plays an important role in maintaining Zn homeostasis and proper β-cell function, avoiding the onset of type 2 diabetes. El Muayed et al. (2010). Journal of Endocrinology, in press.

Read the full article at DOI:10.1677/JOE-09-0420