Fig. 6: Fecal microbiota of Acod1-deficient mice offers transferable protection from metabolic disease by preventing meta-inflammation.

Body (A) and tissue (B) weights of HFD-fed WT and Acod1^-/- mice receiving either PBS (donor) or a fecal suspension from reciprocal genotypes (recipient). Data as mean ± s.e.m from n = 9 (WT donor), n = 11 (Acod1^-/- donor), n = 8 (WT recipient) and n = 10 Acod1^-/- recipient mice from two experiments independently executed. C ITT from mice treated as in A. Data as mean±s.e.m of n = 9 (WT donors), n = 11 (Acod1^-/- donors), n = 8 (WT recipient) and n = 9 Acod1^-/- recipient mice from two experiments independently executed. D Liver triglycerides and (E) qPCR analysis of indicated hepatic genes of mice treated as in A. Data as mean±s.e.m from n = 8 (donors) and n = 7 (recipient) mice from two independent experiments. F Plasma FITC-dextran levels in ND-fed mice and mice treated as in A. Data as mean±s.e.m from n = 4 (ND), n = 7 (WT donor), n = 9 (Acod1^-/- donor), n = 7 (WT recipient), and n = 8 (Acod1^-/- recipient) mice from two independent experiments. G Correlation analysis between mRNA of ACOD1 and the indicated genes in colon specimens of human obese (n = 16) subjects (GSE158237). H qPCR analysis of indicated genes in eWAT of mice treated as in A. Data as mean±s.e.m from n = 8 (donors) and n = 7 (recipient) mice from two independent experiments. I qPCR analysis of indicated genes in BAT of mice treated as in A. Data as mean±s.e.m from n = 7 (WT donor), n = 9 (Acod1^-/- donor) and n = 7 (recipient) mice from two independent experiments. J Diagram summarizing ACOD1-driven metabolic disease sequelae. In (A), (C) two-way ANOVA; In (B), (D–F), (H, I) one-way ANOVA with Dunnett’s multiple comparisons test compared with WT donor; *P < 0.05; **P < 0.01; ***P < 0.001; ns not significant.