| Project/Area Number |
26560059
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Eating habits
|
|---|
| Research Institution | Shizuoka University (2015-2016)
Nayoro City University (2014) |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 水素 / 大腸発酵 / メタボリックシンドローム / 難消化性糖質 / 大腸 / 脂肪組織 / 慢性炎症 / サイトカイン / フラクトオリゴ糖 |
|---|
| Outline of Final Research Achievements |
We examined whether the reducing power of hydrogen molecules (H2) generated by colonic fermentation could suppress inflammation in diet-induced obese rats. Additionally, we sought to determine the minimum amount of fermentation substrate needed to maintain high colonic H2 production for 24 h. We found that a high production of colonic H2 over 24h, derived from the delivery to the large intestine of more non-digestible saccharides than could be used, increased the concentration of H2 in the adipose tissue and suppressed the secretion of IL-6, which is a proinflammatory cytokine. In short, a high H2 production from the large intestine over a 24 h period was achievable when sufficient amounts of non-digestible saccharides were delivered to the large intestine as a fermentation substrate, with the resultant high production of H2 leading to inhibited metabolic syndrome via the alleviation of inflammation.
|
