2002 Fiscal Year Final Research Report Summary
Analysis of pancreatic endocrine function in acute pancreatitis
| Project/Area Number |
12671259
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyorin University |
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Principal Investigator |
ABE Nobutsugu Kyorin University, School of Medicine, Assistant, 医学部, 助手 (40266747)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Hideo Kyorin University, School of Medicine, Assistant, 医学部, 助手 (60333027)
NAGAMATSU Shinya Kyorin University, School of Medicine, Professor, 医学部, 教授 (80231489)
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| Project Period (FY) |
2000 – 2002
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| Keywords | Acute pancreatitis / Endocrine function / GLUT2 |
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| Research Abstract |
An impairment in pancreatic endocrine function is thought to play an important role in the development of glucose intolerance in acute pancreatitis. We investigated the functional aspects of endocrene cells in acute pancreatitis, and the expression of glucose transporter GLUT2 in the pancreatitis islet. A mild form of acute pancreatitis was induced in rat by an injection of a sodium taurocholate solution via a cannulated biliopancreatic duct. To analyze insulin secretion, isolated islets were stimulated by glucose, and insulin secretion was analyzed by radioimmunoassay. Immunohistochemical detection of GLUT2 using a specific antibody was attempted to determine GLUT2 expression in pancreatic islets. A marked elevation of glucose levels observed in the present rat pancreatitis model confirmed that glucose intolerance can occur even in a mild form of pancreatitis. The architecture of the islets, however, remained intact despite marked inflammatory changes in the neighboring exocrine region. Insulin secretion studies revealed that the ability of islets to secrete insulin in response to glucose was markedly reduced in pancreatitis islets. GLUT2 immunoreactivity in endocrine cells was found to be intact in pancreatitis islets. In summary, the amount of insulin released from isolated islets following glucose stimulation is reduced in acute edematous pancreatitis, although pancreatic islets remain histologically intact. Based on the present findings, while the mechanisms responsible for this functional deficiency remain to be determined, the decrease in insulin secretion is possibly caused by impairment of some pancreatic B-cell functions rather than GLUT2-mediated glucose transportation.
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