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Original Articles
- Relationship between Insulin Secretory Capacity and Mitochondrial Morphology in Pancreatic beta-Cell.
- Seung Won Yang, Jae Hyuk Lee, Chang Soo Park, Min Young Chung
- Korean J Pathol. 1999;33(5):326-336.
- 1,711 View
- 22 Download
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Abstract
PDF - To investigate the relationship between insulin response and morphometric changes of the mitochondria of pancreatic beta-cell, this study was performed using hyperglycemia and streptozotocin as oxidative stresses. Adult and neonatal rats were used. Intravenous glucose tolerance test (IVGTT) and morphologic examination of pancreas using immunohistochemical stain, in situ end-labeling method and electron microscopic study were performed. Various mitochondrial parameters were measured by image analyzer. Immunohistochemical stain revealed a markedly reduced islet size and decreased number of beta-cells and the increased number of non-beta-cell in adult and neonatoal streptozotocin group, and the appearance of insulin positive cells throughout the exocrine parenchyma in neonatal streptozotocin group. Three days after injection of streptozotocin in adult streptozotocin group, TUNEL stain showed increased apoptotic cells in islets. Ultrastructurally, beta-cells in adult streptozotocin group showed increase in number and size of mitochondria, and disruption of mitochondrial structures. Hyperglycemic group and neonatal streptozotocin group showed preserved mitochondrial ultrastructure. Ultrastructural morphometric study revealed increase in size and number of mitochondria and decrease in mitochondrial contour index in adult streptozotocin-treated rats, which suggested mitochondrial degeneration. Hyperglycemic group showed mild increase in size of mitochondria. Increased number of mitochondria was also observed in neonatal streptozotocin group. IVGTT revealed marked decrease in insulin response in adult streptozotocin group, and non-insulin-dependent diabetes mellitus pattern in glucose and insulin response in neonatal streptozotocin group. Hyperglycemic group showed a glucose and insulin response similar to control group. The above results suggest that a severe oxidative injury may cause degeneration and disruption of mitochondria of pancreatic beta-cell, and may be associated with substantial apoptotic cell death. The changes in the morphology and the number of mitochondria may result from streptozotocin treatment within neonatal period and hyperglycemia treatment, which may be associated with changes in insulin response.
- The Effect of Aminoguanidine and Insulin on the Development of Insulitis and the Expression of Inducible Nitric Oxide Synthase in Multiple Low Dose Streptozotocin-induced Diabetic Mice.
- Hee Kyung Chang, Ji Young Suh, Young Sik Choi, Soon Young Kim, Chang Hyun Yoo, Bang Hur, Yo Han Park
- Korean J Pathol. 1999;33(6):415-421.
- 1,797 View
- 18 Download
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Abstract
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- In this study the effect of insulin and aminoguanidine on the expression of iNOS and the development of insulitis in the multiple low dose streptozotocin (SZ) induced diabetic (LDSD) mice was evaluated. Eighty mice (Charles-River CD-1 mice) were divided into four groups. Group I received SZ for five days. Group II received SZ for five days and was followed by insulin treatment. Group III received SZ for five days and was followed by aminoguanidine treatment. Group IV was normal control group. The blood glucose level and body weight were measured weekly. On the 35th day, pancreat ic sections were observed to evaluate the frequency and the severity of insulitis in addition to the immunohistochemical expression of iNOS in the pancreatic islets. Blood glucose levels of group IV were significantly lower than other experimental groups on the 21st, 28th, and 35th day. The difference in blood glucose levels was not statistically significant. Incidence of the insulitis was lower in group II than in groups I and III. The severity of insulitis correlated with the increase in blood glucose level only in group II. The expression of iNOS was more pronounced in group I than in groups II and III. Aminoguanidine did not inhibit development of the insulitis but decreased expression of iNOS in the pancreatic islets. Therefore it is speculated that iNOS production is one of the factors and other pathogenetic mechanisms might be involved in the development of insulitis.
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