| Project/Area Number |
26860222
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Nihon University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
MAKISHIMA Makoto 日本大学, 医学部, 教授 (70346146)
HONDA Akira 東京医科大学, 茨城医療センター, 教授 (10468639)
NISHIDA Shigeru 日本大学, 医学部, 准教授 (90211458)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | ビタミンD / 胆汁酸 / 核内受容体 / 肥満 / 腸内細菌 |
|---|
| Outline of Final Research Achievements |
My research goal is to elucidate how vitamin D receptor (VDR) involves in the bile acid metabolism in obesity. Wild-type mice and VDR knockout mice took high fat diet (HFD) or control diet for four weeks. I collected blood plasma, liver, urine and feces samples, and analyzed bile acid composition. HFD decreased plasma taurocholic acid contents and increased contents of unconjugated cholic acid, deoxycholic acid, alpha muricholic acid and beta muricholic acid in feces. Interestingly, VDR deficiency further increased these unconjugated bile acids. The results indicate that VDR is involved in the metabolism of taurocholic acid and that VDR deficiency enhances deconjugation of fecal bile acids, suggesting intestinal bacterial activation.
|
