Islets · 2011
Islet amyloid polypeptide in pancreatic islets from type 1 diabetic subjects.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Rissel René, Moellmann Christian, Albertsmeier Victoria, Renz Miriam, Ruemmler Robert, Kamuf Jens, Hartmann Erik K, Ziebart Alexander
Аннотация
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.
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.