| Project/Area Number |
24580174
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Chiba University |
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Principal Investigator |
OARADA MOTOKO 千葉大学, 真菌医学研究センター, 助教 (40211784)
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| Co-Investigator(Kenkyū-buntansha) |
GONOI Tohru 千葉大学, 真菌医学研究センター, 教授 (30134365)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 栄養学 / 食生活 / 肝臓 / 炎症 / 復食 / 炭水化物 / グルコース / 炎症反応 / 生活習慣病 / TLR2 |
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| Outline of Final Research Achievements |
Unhealthy eating behaviors increase the risk of metabolic diseases, but the underlying mechanisms are not fully elucidated. Because inflammation contributes to the pathogenesis of metabolic diseases, the objective of our present study was to address the effects of a fasting-refeeding regime, a model of irregular eating, on the hepatic inflammatory responses in mouse. Refeeding with a standard diet increased the liver expression of Tlr2 and proinflammatory mediators. These increases were attenuated in mice refed a low-carbohydrate/high-fat diet. TLR2 deficiency significantly attenuated the refeeding-induced increase in the liver expression of inflammatory genes. Dietary glucose, rather than fructose, plays a significant role in this increase. These findings suggest that an irregular eating behavior can elicit a liver inflammatory response, which is at least partly mediated by TLR2, and that dietary carbohydrates play critical roles in this process.
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