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Am J Physiol Endocrinol Metab 278: E684-E691, 2000;
0193-1849/00 $5.00
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Vol. 278, Issue 4, E684-E691, April 2000

Islet amyloid polypeptide (amylin)-deficient mice develop a more severe form of alloxan-induced diabetes

Hindrik Mulder1,2, Samuel Gebre-Medhin3,4, Christer Betsholtz4, Frank Sundler2, and Bo Ahrén5

1 Section for Molecular Signaling, Department of Cell and Molecular Biology, Lund University, SE-221 00 Lund; 2 Section for Neuroendocrine Cell Biology, Department of Physiological Sciences, Lund University, SE-221 85 Lund; 3 Section for Molecular and Cellular Physiology, Department of Physiological Sciences, Lund University, SE-223 62 Lund; 5 Dept. of Medicine at Malmö University Hospital, Lund University, SE-205 02 Malmo; and 4 Dept. of Medical Biochemistry, Göteborg University, SE-405 30 Goteborg, Sweden

To examine whether islet amyloid polypeptide (IAPP), other than through amyloid formation, may be of importance in diabetes pathogenesis, IAPP-deficient mice (IAPP-/-) were challenged with alloxan (day 0). Diabetes in IAPP-/- mice was more severe at day 35, indicated by greater weight loss; glucose levels were higher in alloxan-treated IAPP-/- mice, whereas insulin levels were lower, indicating a greater impairment of islet function. Accordingly, glucose levels upon intravenous glucose challenges at days 7 and 35 were consistently higher in alloxan-treated IAPP-/- mice. At day 35, insulin mRNA expression, but not beta -cell mass, was lower in untreated IAPP-/- mice. Yet, upon alloxan administration, beta -cell mass and numbers of beta -cell-containing islets were significantly more reduced in IAPP-/- mice. Furthermore, they displayed exaggerated beta -cell dysfunction, because in their remaining beta -cells, insulin mRNA expression was significantly more impaired and the localization of glucose transporter-2 was perturbed. Thus the lack of IAPP has allowed exaggerated beta -cell cytotoxic actions of alloxan, suggesting that there may be beneficial features of IAPP actions in situations of beta -cell damage.

gene knockout; beta -cell mass; insulin messenger ribonucleic acid; glucose transporter-2; glucose tolerance


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