Extended Data Figure 6: The gut microbiota drive increased acetate turnover and GSIS.
From: Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome
a, b, Plasma glucose and glucose infusion rate during a hyperglycaemic clamp in rats following faecal transplant replicates acetate turnover and GSIS in the donor group. c, Plasma acetate. d, Faecal acetate concentration. n = 7 (HFD to chow) or 8 (chow to chow, chow to HFD) per group. e, Plasma insulin AUC. f, Glucose-stimulated insulin release in isolated islets incubated with 400 μM acetate in a physiological buffer. n = 4 per group. g, Plasma C2 acetylcarnitine content. h, Glucose-stimulated insulin release in isolated islets incubated with 100 μM acetylcarnitine. i–m, Plasma alanine, leucine, arginine, glucagon, and GLP-1 concentrations. n, o, Plasma glucose and glucose infusion rate during a hyperglycaemic clamp in acetate-infused rats treated with a GLP-1 inhibitor. p, q, Plasma acetate and whole-body acetate turnover. r, s, Plasma insulin and insulin AUC during the clamp. In all panels, data are mean ± s.e.m. of n = 6 per group. In a–e, ****P < 0.0001 versus chow-fed donor to chow-fed recipient transplants; §§§§P < 0.0001 versus chow-fed donor to HFD-fed recipient transplants by one-way ANOVA with Bonferroni’s multiple comparisons test. Data are the mean ± s.e.m. of n = 6 (HFD to chow) or 7 (chow to chow, chow to HFD) per group. In g–m, *P < 0.05, **P < 0.01 versus 2 μmol kg−1 min−1 acetate; §P < 0.05 versus 8 μmol kg−1 min−1 acetate by one-way ANOVA with Bonferroni’s multiple comparisons test. In g–s, data are the mean ± s.e.m. of n = 6 (unless otherwise specified) per group. In n–s, no significant differences were measured by the two-tailed unpaired Student’s t-test.
