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.2011 Jul-Aug;3(4):166-74.
doi: 10.4161/isl.3.4.15875. Epub 2011 Jul 1.

Islet amyloid polypeptide in pancreatic islets from type 1 diabetic subjects

Affiliations

Islet amyloid polypeptide in pancreatic islets from type 1 diabetic subjects

Tatsuo Tomita. Islets.2011 Jul-Aug.

Abstract

Aims/hypothesis: Islet amyloid polypeptide is originally isolated as the chief constituent of amyloid deposits in type 2 diabetic islets. Islet amyloid polypeptide hyposecretion was known in type 1 diabetics and this study aimed to detect possibly reduced islet amyloid polypeptide-positive cells in type 1 diabetic islets.

Results: Non-diabetic control islets showed about 60% of islet cells were insulin cells, and 60% of insulin cells were positive for IAPP. In type 1 diabetic islets, islets were generally smaller than control islets, consisting of weaker positive cells for insulin and islet amyloid polypeptide. Medium-sized islets still retained some insulin positive cells, whereas islet amyloid polypeptide positive cells were much less or even absent, but some insulin-negative cells were weakly islet amyloid polypeptide positive. An occasional extra-large islet, representing regenerating islets, consisting of more than 100 islet cells revealed less than 35% insulin and 20% islet amyloid polypeptide positive cells with relatively increased glucagon and somatostatin cells. Both normal and type 1 diabetic islets revealed scattered, densely insulin and islet amyloid polypeptide positive sickle-shaped cytoplasm without granular appearance, consistent with degenerating insulin cells.

Methods: Using commercially available rabbit anti-islet amyloid polypeptide antibody, immunostaning was performed on ten cases of type 1 diabetic pancreata and eight non-diabetic controls. Both control and type 1 diabetic pancreata were systematically immunostained for insulin, glucagon, somatostatin and islet amyloid polypeptide.

Conclusion/interpretation: Control islets consisted of about 60% insulin cells, and about 34% of islet cells were amyloid polypeptide positive with scattered and densely positive for insulin and islet amyloid polypeptide without granular appearance, consistent with degenerating β cells. All islets, including occasional extra-large islets from type 1 diabetics, showed less insulin cells and less islet amyloid polypeptide positive cells with twice increased glucagon and somatostatin cells of the control islets, but some insulin-negative cells were positive for islet amyloid polypeptide, suggesting the presence of islet amyloid polypeptide in degenerating and extra-large regenerating islets. Thus, this immunocytochemical staining revealed generally less islet amyloid positive cells in type 1 diabetic islets, corresponding to severe hyposecretion of islet amyloid polypeptide in type 1 diabetics.

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Figures

Figure 1
Figure 1
Control islets. Insulin cells were the major islet cells (about 60%) with abundant cytoplasm of variable staining density, followed by glucagon cells with densely stained, smaller cytoplasm (about 30%) and SRIF cells (about 10%). IAPP positive cells with abundant cytoplasm accounted for about 30% of total islet cells. Both insulin and IAPP immunostaining revealed scattered, dense staining in the irregular, sickle-shaped cytoplasm with lesser staining density for IAPP than that of insulin (*). L, large islet, M, medium sized islet. (A) Insulin, (B) IAPP, (C) glucagon and (D) SRIF immunostained.
Figure 2A–D
Figure 2A–D
Type 1 diabetic islets, Case 1 (A–D) and Case 2 (E–H) from patients younger than 40 years of age. Small insulin cells with scanty cytoplasm were minor components and glucagon cells, which were diffusely located in the islets, were the major components at about 66%, whereas IAPP positive cells revealed small and scanty cytoplasm similar to that of insulin cells although IAPP immunostaining was less densely stained than insulin staining in Case 1. (A and E) Insulin, (B and F) IAPP, (C and G) glucagon and (D and H) SRIF immunostained. Type 1 diabetic islets, Case 2 (E–H) from patients younger than 40 years of age. There were no insulin-positive cells in Case 2 but were residual IAPP positive cells in insulin-negative islet cells. SRIF cells were located in mid portion of islets, location of which roughly corresponds to IAPP positive cells. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained.
Figure 2A–D
Figure 2A–D
Type 1 diabetic islets, Case 1 (A–D) and Case 2 (E–H) from patients younger than 40 years of age. Small insulin cells with scanty cytoplasm were minor components and glucagon cells, which were diffusely located in the islets, were the major components at about 66%, whereas IAPP positive cells revealed small and scanty cytoplasm similar to that of insulin cells although IAPP immunostaining was less densely stained than insulin staining in Case 1. (A and E) Insulin, (B and F) IAPP, (C and G) glucagon and (D and H) SRIF immunostained. Type 1 diabetic islets, Case 2 (E–H) from patients younger than 40 years of age. There were no insulin-positive cells in Case 2 but were residual IAPP positive cells in insulin-negative islet cells. SRIF cells were located in mid portion of islets, location of which roughly corresponds to IAPP positive cells. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained.
Figure 3
Figure 3
Type 1 diabetic islets, Case 5. Insulin cells were less numerous than in control islets at moderate granular staining. IAPP positive cells were much less than insulin cells with granular appearance. Both glucagon and SRIF cells were more numerous than in control islets. (A) Insulin, (B) IAPP, (C) Glucagon and (D) SRIF immunostained.
Figure 4
Figure 4
Type 1 diabetic large (A–D) and extra-large islets (E–H), Case 7 from a patient older than 40 years of age. There were more insulin positive cells than IAPP positive cells with stronger staining for insulin than IAPP staining and major glucagon cells were of about equal numbers in large and medium sized islets (A–D) with glucagon cells diffusely distributed. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained. Type 1 diabetic extra-large islets (E–H), Case 7 from a patient older than 40 years of age. In extra-large islets (E–H), weakly stained, granular insulin cells with abundant cytoplasm were less than glucagon and SRIF cells. Both insulin and IAPP immunostaining was weakly granular with scattered irregular sickle-shaped densely dark cytoplasmic staining without granular appearance (*). IAPP immunostained cells with weakly granular staining were relatively more than insulin cells. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained.
Figure 4
Figure 4
Type 1 diabetic large (A–D) and extra-large islets (E–H), Case 7 from a patient older than 40 years of age. There were more insulin positive cells than IAPP positive cells with stronger staining for insulin than IAPP staining and major glucagon cells were of about equal numbers in large and medium sized islets (A–D) with glucagon cells diffusely distributed. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained. Type 1 diabetic extra-large islets (E–H), Case 7 from a patient older than 40 years of age. In extra-large islets (E–H), weakly stained, granular insulin cells with abundant cytoplasm were less than glucagon and SRIF cells. Both insulin and IAPP immunostaining was weakly granular with scattered irregular sickle-shaped densely dark cytoplasmic staining without granular appearance (*). IAPP immunostained cells with weakly granular staining were relatively more than insulin cells. (A and E) Insulin, (B and F) IAPP, (C and G) Glucagon and (D and H) SRIF immunostained.
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