| Project/Area Number | 04670810 |
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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 | KANAZAWA MEDICAL UNIVERSITY |
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Principal Investigator |
KINAMI Yoshio KANAZAWA MEDICAL UNIVERSITY・MEDICAL RESEARCH INSTITUTE・PROFESSOE, 総合医学研究所, 教授 (00019928)
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| Co-Investigator(Kenkyū-buntansha) |
SETO Keitaro KANAZAWA MEDICAL UNIVERSITY・SCHOOL OF MEDICINE・ASSISTANT, 医学部, 助手 (40216544)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed(Fiscal Year 1994)
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| Budget Amount *help |
¥2,200,000 (Direct Cost : ¥2,200,000)
Fiscal Year 1994 : ¥800,000 (Direct Cost : ¥800,000)
Fiscal Year 1993 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1992 : ¥700,000 (Direct Cost : ¥700,000)
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| Keywords | Cholangiocarcinoma / Bile Acid Load / Deoxycholic Acid / Diisopropanolnitrosamine / deoxycholic acid. |
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| Research Abstract |
This study was performed to clarify the promoting effects of primary or secondary bile acid load on the occurrence of cholangiocarcinoma, using Syrian golden hamsters. These hamsters received subcutaneously diisopropanolnitrosamine (DIPN) once weekly for 10 weeks, and simultaneously were given a standard pellet diet (control group) containing taurocholic acid (TCA group) or deoxycholic acid (DCA group). The rates of cholangiocarcinoma at 20 weeks were 23% in the control group, 60% in the TCA group and 59% in the DCA group. There were significant differences between the control and the TCA or DCA groups (p<0.05). The rates of proliferation of bile ductules or hyperplasia of the bile duct epithelium and the bromodeoxyuridine labeling indices of bile duct epithelial cells were high in both groups treated with bile acids, compared with those in the control group. Regarding the composition of bile acids in the intraductal bile, the TCA and DCA groups revealed a decrease in primary bile acids and an increase in DCA.These results suggest that both TCA and DCA given orally promote the occurrence of DIPN-induced cholangiocarcinoma.
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