morphological signs of membrane damage and are most probably not functioning in a normal way. Therefore, the functional b-cell mass may be very different from the total b-cell mass. A morphological measurement of the total b-cell mass does not give true functional mass. Amyloid in transplanted human islets Human islets isolated from organ donors may be transplanted to diabetic recipients, particularly in cases with diabetes which is difﬁcult to regulate with the common regimens. Most commonly this is done via an islet infusion into the portal vein. Initially, many patients become independent of exogeneous insulin injections, but most commonly the function of the grafted islets deteriorates with time, and after a few years most individuals need insulin treatment (recently reviewed in (74)). Pioneered by Andersson (75), human islets can be isolated and transplanted into nude mice, some of which were made diabetic by means of alloxan injections. We found that normal human islets, transplanted under the kidney capsule (45) or into the spleen or liver (76), rapidly develop amyloid deposits. We therefore questioned whether amyloid may form also in clinically transplanted islets (77). Recently, we had the opportunity to study the liver of one patient who had been transplanted 5 years earlier and who died from a cardiac infarction. Indeed, almost 50% of the studied islets contained IAPP amyloid, often in a substantial amount (78). This ﬁnding has recently been veriﬁed by studies of additional cases (Westermark et al., unpublished). Therefore, by transplantation of normal human islets into type 1 diabetic individuals, type 2 diabetic alterations are induced in these islets. Conclusion Porte pointed out two ﬁndings in type 2 diabetes, providing clues to the pathogenesis: the relative hyperproinsulinemia and the deposits of amyloid in the islets (79). Hyperproinsulinemia would most likely be associated with aberrant cleavage also of pro- IAPP. There is evidence that the aberrant cleavage product may start amyloid deposition by the forma- tion of a nucleus (46,52). The amyloid formed may cause b-cell apoptosis and dysfunction of remaining cells. These mechanisms may also be important for the loss of function of transplanted human islets. Acknowledgements I have had the privilege to work with a large number of researchers over the years. A list of the names would Amyloid in the islets of Langerhans 87 be too long, but I would like to take the opportunity to thank them all. Declaration of interest: Own research was sup- ported by the Swedish Research Council, the Swedish Diabetes Association, and the Family Ernfors Fund. The author alone is responsible for the content and writing of the paper. References 1. Westermark P, Wernstedt C, Wilander E, Sletten K. 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