Imidazole propionate {90000174} Record Keys Parent:[ ] Definition:Imidazole propionate Queue:[ ] Details Initialisation date:[ ] Specification: [ ]Source: [ ] Meta Information Structural Type:[ ] Functional Type:[ ] Function:[ ] Notes: [ ]Shared Reference Notes [1.1] [#Diabetes Type 2] - The microbial product of histidine metabolism, imidazole propionate (ImP), was recently shown to be directly involved in insulin resistance. - Exogenous ImP showed worsened glucose tolerance, increased gluconeogenic enzyme expression, increased S6 kinase phosphorylation, and impaired insulin signaling in multiple tissues on a normal chow diet. In vitro ImP also impaired insulin-stimulated phosphorylation of protein kinase B. - ImP activates mTORC1. [1.2] [#Diabetes Type 2] - #Dimethylglycine, imidazole propionate, #Tryptophan, #kynurenine and #Indolelactate associated with increased risk of T2D [1.3] [#Diabetes Type 2] - Imidazole propionates (ImP), produced by several bacterial strains, including #Streptococcus mutans and #Eggerthella lenta, which was found to be elevated in individuals with T2DM and impairs insulin signaling through activation of the p38γ-p62-mTORC1 pathway [1.4] [#Diabetes Type 2] - CACS-associated species were also found positively associated with imidazole propionate, a microbially derived metabolite from #Histidine, reported to impair #Glucose metabolism. [1.5] [#Diabetes Type 2] - #Histidine is the source Imidazole Propionate metabolite. It is negatively correlated with diabetes. - It hampers #Glucose tolerance, insulin signaling, #Glucose metabolism disorder, and causes systemic inflammation. [1.6] [#Diabetes Type 2] - imidazole propionate is produced at higher concentrations from #Histidine in a gut simulator when fecal microbiota from T2DM patients is used, and that it impairs #Glucose tolerance when administered to mice. [#Diabetes Type 2] - Imidazole propionate inhibits insulin signal transduction at the receptor level by activating p38 mitogen-activated protein kinase (MAPK), promoting p62 phosphorylation, and then activating the mechanical target of rapamycin complex 1 (mTORC1), which may contribute to T2DM pathogenesisReferences Notes[ ]
