Studies on prevention of obesity-induced low-grade inflammation through improving the profile of gut microbiota by potential probiotic which binds to sulfated sugar chains
| Project/Area Number |
15K07709
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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 |
Animal production science
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| Research Institution | Kitasato University |
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Principal Investigator |
Mukai Takao 北里大学, 獣医学部, 教授 (20229917)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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 | 乳酸菌 / 腸内細菌 / 肥満 / 腸管バリア機能 / ムチン / プロバイオティクス / ビフィズス菌 / 炎症 / 腸管バリア |
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| Outline of Final Research Achievements |
Intestinal epithelial barrier dysfunction and increased permeability is supposed to cause microbial or microbial components translocation which may induce low-grade inflammation in various diseases. It has also been suggested that high-fat diet-induced obesity causes gut dysbiosis that drives inflammation in various diseases. Moreover, the relation of gut dysbiosis to intestinal barrier dysfunction has gradually been clarified, but mechanisms are unknown.
This study strongly suggested that potential probiotic which binds to sulfated sugar chains found in gut mucin prevents intestinal epithelial barrier dysfunction through improving the profile of gut microbiota in high-fat diet-induced obesity model mouse. Furthermore, we suggest a novel mechanism for barrier dysfunction on a high-fat diet involving the effect of metabolites of cholic acid which is one of bile acids by gut microbiota.
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Report
(4 results)
Research Products
(13 results)
