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자료유형
학술저널
저자정보
Heetae Lee (Sahmyook University) Jiyeon Kim (Sahmyook University) Jinho An (Sahmyook University) Sungwon Lee (Sahmyook University) Dohyun Choi (Sahmyook University) Hyunseok Kong (Sahmyook University) Youngcheon Song (Sahmyook University) Il Ho Park (Sahmyook University) Chong-Kil Lee (Chungbuk National University) Kyungjae Kim (Sahmyook University)
저널정보
대한면역학회 Immune Network Immune Network Vol.19 No.4
발행연도
2019.8
수록면
69 - 77 (9page)

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IL-18 is a crucial pro-inflammatory cytokine that mediates chronic intestinal inflammation. Metformin, an anti-diabetic drug, was reported to have ameliorative effects on inflammatory bowel disease. Recently, the mechanism of action of metformin was explained as a modulation of gut microbiota. In this study, fecal microbiota transplantation (FMT) using fecal material from metformin-treated mice was found to upregulate the expression of GLP-1 and pattern-recognition receptors TLR1 and TLR4 for the improvement in hyperglycemia caused by a high-fat diet. Further, FMT downregulated the expression of the inflammatory cytokine IL-18. Within the genera Akkermansia, Bacteroides, and Butyricimonas, which were promoted by metformin therapy, Butyricimonas was found to be consistently abundant following FMT. Our findings suggest that modulation of gut microbiota is a key factor for the anti-inflammatory effects of metformin which is used for the treatment of hyperglycemia.

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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2019-517-001220096