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Fig. 4 | Microbiome

Fig. 4

From: Deficiency of exchange protein directly activated by cAMP (EPAC)-1 in mice augments glucose intolerance, inflammation, and gut dysbiosis associated with Western diet

Fig. 4

Obesity-related phenotypes and gut permeability changes following 8-week WD. All mice were 16-week-old (8-week-old + RD or WD for 8 weeks). a Body weight of WT, Epac1–/–, and Epac2–/– mice while feeding WD over 8 weeks (n = 9–11/genotype/diet). b Blood sugar concentrations in WT, Epac1–/–, and Epac2–/– mice during an oral glucose tolerance test (OGTT) (n = 8–9/genotype/diet). c In vivo gut permeability test (n = 7–8/genotype/diet); RD-fed mice (left panel) and WD-fed mice (right panel); AU, arbitrary unit. d Scatterplots showing relative mRNA levels of jejunal cell-cell TJ markers, ZO-1 (top panels), and occludin (bottom panels) (n = 4–6/genotype/diet). e Representative Western blot image showing Epac1 protein expression was detected in the jejunum of RD and WD-fed WT and Epac2–/– mice, but not Epac1–/– mice (top panel). Scatterplots showing quantification of Epac1 protein expression in the jejunum of WT and Epac2–/– mice (n = 3/genotype/diet) (bottom left panel), and all mice regardless of genotype fed RD or WD (n = 6/diet) (bottom right panel). All data are presented as mean ± SEM. Statistical significance was assessed by two-way ANOVA with Tukey’s post hoc test (a, b); one-way ANOVA with Tukey’s post hoc test and unpaired Student’s t test for comparison between 3 and 2 groups, respectively, *p<0.05 (c–e)

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