2016 Fiscal Year Final Research Report
Novel mechanism analysis of microcystin on organ dysfunction-focusing on bile acid metabolism-
| Project/Area Number |
15K12352
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Eating habits
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| Research Institution | Shimane University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SUGIURA NORIO 筑波大学, 生命環境系, 名誉教授 (10302374)
MIYAZAKI HITOSHI 筑波大学, 生命環境系, 教授 (40183636)
ISHIZUKA SATOSHI 北海道大学, 大学院農学研究院, 准教授 (00271627)
FUKITANI SATORU 北海道大学, 大学院農学研究院, 講師 (10370157)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | ミクロシスチン / 藍藻類由来毒素 / アオコ / 健康リスク評価 / 消化管 / 飲料水 / 淡水魚介類 / 湖沼 |
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| Outline of Final Research Achievements |
Eutrophication of lake and reservoir accelerates development of Microcystis which produces a toxin, called microcystin. The present study shows that in a cultured hepatocyte cell line, HepG2 cells, AMPK was time- and dose-dependently activated by microcystin-LR (MC-LR) stimulation. When AMPK was not activated in MC-LR-treated HepG2 cells, cell death was induced. However, when MC-LR activated AMPK, cell death was inhibited. In a cultured intestinal cell line, Caco-2 cells, MC-LR leaded to cell proliferation through p38 and JNK activation although ERK activation was not participate. Furthermore, the expression levels of oncogene was upregulated in MC-LR-treated Caco-2 cells. In rat analysis, food intake, body weight, and weight of liver, kidney, and adipose tissue were not difference between control and MC-LR-administrated rats. We will continue to check for serum parameter (ALT/AST, TG, and TC etc), liver TG and TC, and gut microbiota, etc.
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| Free Research Field |
病態生理学・分子栄養学
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