| Project/Area Number |
15K00820
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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 |
Eating habits
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KATAOKA Keiko 徳島大学, 大学院医歯薬学研究部(医学系), 教授 (40189303)
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| Co-Investigator(Kenkyū-buntansha) |
櫻井 明子 徳島大学, 大学院医歯薬学研究部(医学系), 助教 (70707900)
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| Research Collaborator |
MORIMOTO Yuuri 徳島大学, 院生
MORIKI Misato 徳島大学, 院生
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 高脂肪高ショ糖食 / 脂肪性肝疾患 / マウス生育時期 / 食餌スタイル / 糞便菌叢 / 腸内環境 / Clostridium / Bifidobacterium / 食餌誘導性肥満モデル / 脂肪肝炎 / 食生活スタイル / 成育段階 / 高脂肪高ショ糖食、 / 脂肪肝 / インスリン抵抗性 / 腸内菌叢 / Bacteroides / 発症リスク |
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| Outline of Final Research Achievements |
High-fat high-sucrose diet (HFHSD) induced changes of gut microbiota composition including increase of a kind of Clostridium and decrease of Bacteroides and Bifidobacterium, followed by increasing fasting blood glucose and fatty liver disease. Feeding HFHSD from weaning period easily affected gut microbiota composition and increased serum biomarkers of the disease in all mice of the group, while wide inter-individual variation was observed in matured and aged mice. However, intervention such as an addition of fermented brown rice to the HFHSD or alternate feeding between HFHSD and normal diet have lowered the serum biomarkers of liver damage, and also affected gut microbiota composition. These results suggest the serious effect of HFHSD on the risk of fatty liver disease if it started from weaning period, and that intervention to the diet component or the style of diet intake have the possibility to decrease the disease risk via microbiota modification.
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