| Project/Area Number |
11670494
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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 |
Gastroenterology
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| Research Institution | Shiga University of Medical Sciences |
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Principal Investigator |
SATO Hiroshi Faculty of Medicine, Department of Biology, Shiga University of Medical Sciences, Professor, 医学部, 教授 (90090430)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | UDP-glucuronosyltransferase / Gene / Drug side effects / Polymorphism / 多型 / 薬剤 / 副作用 |
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| Research Abstract |
In this study we clarified the following points.
(1) The inhibitory effect of troglitazone (anti diabetic agent) on UDP-glucuronosyltransferase (UGT) activity may lead to toxicity from many compounds metabolized by UGT 1A6 in patients with inherently reduced UGT1A6 activity and the effect of other thioazolidione anti diabetic agents ma be similar.
(2) Chemotherapy for malignant neoplasms sometimes causes unconjugated hyperbilirubinemia in the absence of liver dysfunction. Gene analysis of the two leukemic patients in whom chemotherapy resulted in hyperbilirubinemic response revealed an identical heterozygous missense mutation (G71R). This mutation may be the basis of chemotherapy-induced unconjugated hyperbilirubinemia.
(3) Since anorexia nervosa natients are in a fasting state, they may show moderate unconjugated hyperbilirubinemia if they have Gilbert syndrome. Homozygous missense mutations of the UDP-glucuronopsyltransferase gene cause not only Crigler-Najjar syndrome but also Gilbert syndrome.
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