1999 Fiscal Year Final Research Report Summary
Regeneration of Pancreatic β-cells
| Project/Area Number |
09557073
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
内分泌・代謝学
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| Research Institution | Gunma University |
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Principal Investigator |
KOJIMA Itaru Professor, Department of Cell Biology Institute for Molecular & Cellular Regulation, Gunma University, 生体調節研究所, 教授 (60143492)
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| Co-Investigator(Kenkyū-buntansha) |
MASHIMA Hirosato Assistant Professor, Department of Cell Biology Institute for Molecular & Cellular Regulation, Gunma University, 生体調節研究所, 助手 (10261869)
SHIBATA Hiroshi Associate Professor, Department of Cell Biology Institute for Molecular & Cellular Regulation, Gunma University, 生体調節研究所, 助教授 (20235584)
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| Project Period (FY) |
1997 – 1999
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| Keywords | pancreatic β cells / regeneration / stem cell / diabetes / insulin / islet |
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| Research Abstract |
We studied differentiation factors involved in the formation of pancreatic beta cells using AR42J cells as a model system. We showed that activin A and betacellulin are able to induce differentiation into insulin-producing cells. To determine whether or not these two factors are involved in the differentiation of pancreatic beta cells, we then studied the expression of these factors in the regenerating pancreas. Activin A was expressed in ductal cells of the pancreas and in newly-formed endocrine cells. Betacellulin was expressed in newly-formed endocrine cells. These results are consistent with the notion that these two factors are involved in the islet neogenesis. We therefore examined whether or not these factors are effective in promoting islet neogenesis. We found that exogenous activin A was not effective. However, betacellulin was quite effective in promoting islet neogenesis. Thus, Betacellulin enhanced the formation of endocrine cells in 90% pancreatectomized rats and increased the number of islets in remnant pancreas. Furthermore, plasma glucose after the administration of ip glucose was lower in betacellulin-treated rats and the plasma insulin concentrations were higher in betacellulin-treated rats. Betacellulin also increased the insulin content of the remnant pancreas. These results indicate that betacellulin is effective in promoting regeneration of pancreatic islets after 90% pancreatectomy. Betacellulin is a potential factor to promote islet regeneration.
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[Publications] Ishiyama, N., Kanzaki, M., Seno, M., Yamada, H., Kobayashi, I. and Kojima, I.: "Studies on the betacellulin receptor in pancreatic AR42J cells."Diabetologia. 41. 623-628 (1998)
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[Publications] Mashima, H., Yamada, S., Tajima, T., Seno, M., Yamada, H., Takeda, J. and Kojima, I.: "Genes expressed during the differentiation of pancreatic A42J cells into insulin-secreting cells."Diabetes. 48. 304-309 (1999)
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[Publications] Tada, H., Sasada, R., Kawaguchi, Y., Kojima, I., Gullick, W.J., Salomon, D., Igarashi, K., Seno, M. and Yamada, H.: "Processing and juxtacrine activity of membrane-anchored betacellulin."J. Cell. Biochem.. 72. 423-434 (1999)
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[Publications] Shiozaki, T., Tajima, T., Zhang, Y.Q., Furukawa, M., Nakazato, Y. and Kojima, I.: "Impaired differentiation of endocrine and exocrine cells of the pancreas in transgenic mice expressing the truncated type II activin receptor."Biochem. Biophys. Acta. 1450. 1-11 (1999)
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