Microbially produced imidazole propionate impairs insulin signalling through activation of the p38/p62/mTORC1 pathway > 세미나

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Microbially produced imidazole propionate impairs insulin signalling t…

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  • 2018-01-25

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[BK21 Plus Seminar]

▶Subject: Microbially produced imidazole propionate impairs insulin signalling through activation of the p38/p62/mTORC1 pathway

▶Speaker: Ara Koh Ph.D. (Sahlgrenska hospital of Gothenburg University)
       
▶Date: 2:00 PM/Jan. 30(Tue.)/2018
               
▶Place: Conference room(#179), Postech Biotech Center

▶Abctract
Department of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden
Interactions between the gut microbiota, diet and the host potentially contribute to the development of metabolic diseases, but the underlying mechanisms are unclear. Here, we show that the microbially produced histidine-derived metabolite imidazole propionate: (1) is present at higher concentrations in subjects with type 2 diabetes; (2) is produced from histidine in a gut simulator at higher concentrations when using fecal microbiota from subjects with versus without type 2 diabetes; and (3) impairs glucose tolerance when injected into mice. We further show that imidazole propionate impairs insulin signaling at the level of insulin receptor substrate through the activation of p38 MAPK, which promotes p62 phosphorylation and, subsequently, activation of mechanistic target of rapamycin complex 1 (mTORC1); we also demonstrate increased activation of p62/mTORC1 in liver from subjects with type 2 diabetes. Together, these findings indicate that the microbial metabolite imidazole propionate may contribute to the pathogenesis of type 2 diabetes.

▶Inquiry: Prof. Sung Ho Ryu (279-2292)

* This seminar will be given in English.
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