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. 2012 Jan 17;61(2):364–371. doi: 10.2337/db11-1019

FIG. 6.

FIG. 6.

ffar2 and ffar3 knockout mice have impaired glucose tolerance. A: Glucose stimulated GLP-1 secretion in vivo. ffar2−/− and ffar3−/− mice and wild-type littermates (n = 5 each) were dosed with DPP4 inhibitor at a dose of 20 mg/kg per os after a 4-h fast. Thirty minutes post–DPP4 inhibitor dosing, mice were dosed with 1.5 g/kg glucose per os Plasma active GLP-1 was assessed by a MesoScale assay at 0 and 30 min of the oral glucose tolerance test. Data represent means ± 1 SEM, and statistical significance was assessed by Student t test: *P < 0.05 and **P < 0.01. B–E: Oral glucose tolerance test in ffar2−/− mice (n = 8) (left panel) and wild-type littermates (n = 11) (B and D) or ffar3−/− mice (n = 7) (right panel) and wild-type littermates (n = 6) (C and E). Following an overnight fast, mice were given 1.5 g/kg glucose per os, and blood glucose (B and C) and insulin (D and E) were measured at the time points indicated. F and G: Insulin tolerance test in ffar2−/− mice (n = 11) (left panel) and wild-type littermates (n = 6) (F) or in ffar3−/− mice (n = 7) (right panel) and wild-type littermates (n = 7) (G). Following a 4-h fast, mice were given 0.75/kg insulin intraperitoneal, and blood glucose was measured at the time points indicated. No significant differences between genotypes were observed. Data in B–G represent means ± 1 SEM, and statistical significance was assessed by two-way ANOVA with repeated measures: * P < 0.05, ** P < 0.01, and *** P < 0.001.