2022 Fiscal Year Final Research Report
Identification of microbiota-associated metabolite which protects against
Project/Area Number |
20H03490
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Review Section |
Basic Section 49050:Bacteriology-related
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Research Institution | Keio University |
Principal Investigator |
Kim Yun-Gi 慶應義塾大学, 薬学部(芝共立), 教授 (00620220)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 腸内細菌 / 肥満 / 代謝物 |
Outline of Final Research Achievements |
Obesity is on the rise worldwide and is known to increase the risk of fatal chronic diseases. Therefore, the control of obesity has become an extremely important issue in preventive medicine. In recent years, it has been strongly suggested that gut microbiota are deeply involved in the control of obesity. In this study, we have found that obesity pathophysiology is strongly suppressed in the mice fed a high-fat diet by changing the composition of gut microbiota (obesity-resistant mice). Furthermore, through integrated omics analysis using the obesity-resistant mice, we were able to identify novel gut microbes and their metabolites correlated with the suppression of obesity.
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Free Research Field |
腸内細菌学
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Academic Significance and Societal Importance of the Research Achievements |
腸内細菌叢が宿主の代謝機能に影響を与えていることが次第に明らかになってきたが、腸内細菌による肥満抑制の詳細なメカニズムについては不明な点が多く残されている。そのため、我々は肥満の制御に関わる腸内細菌およびその代謝物を探索し、その作用メカニズムを解明したいと考えた。本研究により、腸内細菌叢を変化させることにより高脂肪食負荷後の体重増加や耐糖能の悪化が強く抑制される肥満抵抗性マウスを作製することができた。この肥満抵抗性マウスを解析することで、宿主の代謝機能低下を抑制する未同定の腸内細菌由来の代謝物およびその作用メカニズムを明らかにできる可能性があり、学術的・社会的意義は非常に高いと考えている。
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