Further evidence for amyloid deposition in clinical pancreatic islet grafts

Gunilla T. Westermark, Alberto M. Davalli, Antonio Secchi, Franco Folli, Tatsuya Kin, Christian Toso, A. M James Shapiro, Olle Korsgren, Gunnar Tufveson, Arne Andersson, Per Westermark

Research output: Contribution to journalArticlepeer-review


Background. The reasons for the long-term complete or partial loss of islet graft function are unknown, but there are obviously other reasons than just pure allogeneic graft rejection. Earlier studies have shown that deposition of islet amyloid polypeptide amyloid in transplanted islets may indicate a mechanism for loss of β cells. Materials and Methods. Sections from liver material from four deceased islet-bearing recipients have been scrutinized for the presence of amyloid. Clinical data and certain aspects of the islet graft pathology of these patients have been published previously. RESULT.: With this extended histological analysis, we demonstrate the occurrence of amyloid deposits in islets transplanted into the liver in three of four patients with type 1 diabetes. Conclusion. The finding adds evidence to the assumption that aggregation of islet amyloid polypeptide might be an important cause of progressing β-cell dysfunction in clinically transplanted islets.

Original languageEnglish
Pages (from-to)219-223
Number of pages5
Issue number2
Publication statusPublished - Jan 27 2012


  • Beta cell
  • Islet amyloid
  • Islet graft
  • Transplant pathology
  • Type 1 diabetes

ASJC Scopus subject areas

  • Transplantation


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