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. Author manuscript; available in PMC: 2018 Feb 28.
Published in final edited form as: Nature. 2017 Aug 30;549(7670):48–53. doi: 10.1038/nature23874

Figure 5. N-acyl serinols affect GLP-1 secretion in vitro and glucose homeostasis in vivo.

Figure 5

a, β-arrestin GPR119 activation assay using microbiota (green) and human (blue) ligands (each dose performed in duplicate). b, β-arrestin assay comparing microbiota ligands and 20 synthesized N-palmitoyl amino acids (screen performed in singlicate). c, Release of GLP-1 by GLUTag cells (ANOVA, p < 0.05, data combined from 2 independent experiments, N = 4 for DMSO and 2-oleoyl glycerol, N = 6 for OEA and N-oleoyl serinol). d, Oral glucose tolerance test (OGTT) in gnotobiotic mice. Treatment mice (n = 6 mice, data combined from 2 independent experiments) were colonized with E. coli producing N-acyl serinols and control mice (n = 8 mice, data combined from 2 independent experiments) were colonized with E. coli containing an empty vector (two way ANOVA, bonferroni post-hoc) e, OGTT after withholding IPTG to stop N-acyl gene expression (no difference, two way ANOVA, N is the same as in d). f, OGTT in an antibiotic treated mouse cohort (n = 9 mice in both groups, data combined from 2 independent experiments, two way ANOVA, bonferroni post-hoc). g, Insulin (n = 6 mice in both groups, one experiment, technical triplicates) and h, GLP-1 (n = 9 control mice, n = 10 treatment mice, data combined from 2 independent experiments, technical replicates) measured at 15 min after glucose gavage in the antibiotic treated cohort (unpaired T test, two tailed). Key Bacterial (green) and human (blue) GPR119 ligands reference figure colors. Error bars (mean +/− SEM) * p < 0.05, ** p < 0.01 *** p < 0.001.