期刊
MICROBIOLOGY AND IMMUNOLOGY
卷 55, 期 11, 页码 774-782出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1348-0421.2011.00382.x
关键词
5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR); adenosine monophosphate-activated protein kinase (AMPK); diabetes; metformin
资金
- Japan Society for the Promotion of Science
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Ministry of Health, Labor and Welfare, Japan
- JST/JICA SATREPS
- Yakult Foundation
- University of Fukui
- Organization for Life Science Advancement Programs
- Grants-in-Aid for Scientific Research [22590285, 22591105] Funding Source: KAKEN
Persistent infection with hepatitis C virus (HCV) is closely correlated with type 2 diabetes. In this study, replication of HCV at different glucose concentrations was investigated by using J6/JFH1-derived cell-adapted HCV in Huh-7.5 cells and the mechanism of regulation of HCV replication by AMP-activated protein kinase (AMPK) as an energy sensor of the cell analyzed. Reducing the glucose concentration in the cell culture medium from 4.5 to 1.0 g/L resulted in suppression of HCV replication, along with activation of AMPK. Whereas treatment of cells with AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) suppressed HCV replication, compound C, a specific AMPK inhibitor, prevented AICAR's effect, suggesting that AICAR suppresses the replication of HCV by activating AMPK in Huh-7.5 cells. In contrast, compound C induced further suppression of HCV replication when the cells were cultured in low glucose concentrations or with metformin. These results suggest that low glucose concentrations and metformin have anti-HCV effects independently of AMPK activation.
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