Experimental Diabetes Research
Volume 2008 (2008), Article ID 562985, 8 pages
doi:10.1155/2008/562985
Review Article

Amyloid Deposition in Transplanted Human Pancreatic Islets: A Conceivable Cause of Their Long-Term Failure

1Department of Medical Cell Biology, Uppsala University, 751 23 Uppsala, Sweden
2Division of Cell Biology, Diabetes Research Centre, Linköping University, 581 83 Linköping, Sweden
3Department Genetics and Pathology, Uppsala University, 751 85 Uppsala, Sweden

Received 28 March 2008; Revised 30 June 2008; Accepted 1 December 2008

Academic Editor: Steven E. Kahn

Copyright © 2008 Arne Andersson et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Following the encouraging report of the Edmonton group, there was a rejuvenation of the islet transplantation field. After that, more pessimistic views spread when long-term results of the clinical outcome were published. A progressive loss of the β-cell function meant that almost all patients were back on insulin therapy after 5 years. More than 10 years ago, we demonstrated that amyloid deposits rapidly formed in human islets and in mouse islets transgenic for human IAPP when grafted into nude mice. It is, therefore, conceivable to consider amyloid formation as one potential candidate for the long-term failure. The present paper reviews attempts in our laboratories to elucidate the dynamics of and mechanisms behind the formation of amyloid in transplanted islets with special emphasis on the impact of long-term hyperglycemia.