Zinc and Zinc Transporter Regulation in Pancreatic Islets and the Potential Role of Zinc in Islet Transplantation

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The Review of Diabetic Studies,2010,7,4,263-274.
Published:February 2011
Type:Review Article
Author(s) affiliations:

Mariea D. Bosco1, Daisy M. Mohanasundaram1, Chris J. Drogemuller1, Carol J. Lang2,3, Peter D. Zalewski2,3, and P. Toby Coates1,2,4

1Central Northern Adelaide Renal and Transplantation Service, Renal and Transplantation Immunology Lab, Royal Adelaide Hospital, Adelaide, South Australia 5000.

2School of Medicine, University of Adelaide, South Australia.

3Chronic Inflammatory Disease Research Group, The Queen Elizabeth Hospital, South Australia.

4Centre for Stem Cell Research, University of Adelaide, South Australia.


The critical trace element zinc is essential for normal insulin production, and plays a central role in cellular protection against apoptosis and oxidative stress. The regulation of zinc within the pancreas and β-cells is controlled by the zinc transporter families ZnT and ZIP. Pancreatic islets display wide variability in the occurrence of these molecules. The zinc transporter, ZnT8 is an important target for autoimmunity in type 1 diabetes. Gene polymorphisms of this transporter confer sensitivity for immunosuppressive drugs used in islet transplantation. Understanding the biology of zinc transport within pancreatic islets will provide insight into the mechanisms of β-cell death, and may well reveal new pathways for improvement of diabetes therapy, including islet transplantation. This review discusses the possible roles of zinc in β-cell physiology with a special focus on islet transplantation.