| Project/Area Number |
05671044
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | Teikyo University |
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Principal Investigator |
SUGIYAMA Masanori Teikyo University Department of Surgery, Associated Professor, 医学部, 講師 (20192825)
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| Co-Investigator(Kenkyū-buntansha) |
NAKA Shuji Teikyo University Department of Surgery, Assistant Doctor, 医学部, 助手 (60256063)
NAGASHIMA Yoshitsugu Teikyo University Department of Surgery, Associated Professor, 医学部, 講師 (80198324)
KOZAWA Kunihisa Teikyo University Department of Surgery, Assistant Professor, 医学部, 助教授 (90192054)
WADA Nobuaki Teikyo University Department of Surgery, Professor, 医学部, 教授 (80092386)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | chronic pancreatitis / pancreatic exocrine function / protease inhibitor / animal model |
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| Research Abstract |
The effect of oral administration of protease inhibitor (camostat) on pancreatic morphology and exocrine function (conscious-rat model) was investigated using WBN/Kob rats with spontaneous chronic pancreatitis. In nontreated WBN/Kob rats (2 to 12 months of age), pancreatic fibrosis and parenchymal destruction compatible with human chronic pancreatitis appeared at 3 months and advanced with each month. Pancreatic secretion was markedly impaired at all ages. In WBN/Kob rats fed diets containing camostat (from 2 to 3, or from 4 to 5 months of age), the pancreas was hypertrophic but did not show any histological appearances compatible with chronic pancreatitis, and moreover, exocrine funciton was thoroughly restored with increased plasma cholecystokinin concentrations. Oral administration of protease inhibitor has both preventive and therapeutic effects on pancreatic lesions and dysfunction in an animal model of chronic pancreatitis, probably via endogenous cholecystokinin release.
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