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- W2611193889 abstract "Glucagon-like peptide-1 (GLP-1)-based therapies control glycemia in type 2 diabetic (T2D) patients. However, in some patients the treatment must be discontinued, defining a state of GLP-1 resistance. In animal models we identified a specific set of ileum bacteria impairing the GLP-1-activated gut-brain axis for the control of insulin secretion and gastric emptying. Using prediction algorithms, we identified bacterial pathways related to amino acid metabolism and transport system modules associated to GLP-1 resistance. The conventionalization of germ-free mice demonstrated their role in enteric neuron biology and the gut-brain-periphery axis. Altogether, insulin secretion and gastric emptying require functional GLP-1 receptor and neuronal nitric oxide synthase in the enteric nervous system within a eubiotic gut microbiota environment. Our data open a novel route to improve GLP-1-based therapies." @default.
- W2611193889 created "2017-05-12" @default.
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- W2611193889 date "2017-05-01" @default.
- W2611193889 modified "2023-10-14" @default.
- W2611193889 title "A Specific Gut Microbiota Dysbiosis of Type 2 Diabetic Mice Induces GLP-1 Resistance through an Enteric NO-Dependent and Gut-Brain Axis Mechanism" @default.
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- W2611193889 doi "https://doi.org/10.1016/j.cmet.2017.04.013" @default.
- W2611193889 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28683293" @default.
- W2611193889 hasPublicationYear "2017" @default.
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