Fig. 7

RYGB microbiota requires intestinal FXR and systemic TGR5 signaling to transfer metabolic health benefits in HFD-induced obesity. a–d Relative mRNA expression of FXR target genes in ileum (a), relative body weight change (in %; øBW per group: FMT(Gly-MCA) W0: 29.3 g, W5: 35.7 g; FMT^RYGB W0: 28.4 g, W5: 31.4 g) (b), and epididymal (eWAT) (c) and inguinal (iWAT) white fat mass (WAT) (d) relative to body weight of HFD-fed mice at 5 weeks of RYGB fecal microbiota transfer (FMT^RYGB) co-treated with Gly-MCA (FMT(Gly-MCA)) compared to FMT control mice without co-treatment with Gly-MCA (FMT^RYGB). e-h Oral glucose-tolerance tests (oGTT) (e) and insulin-sensitivity tests (ITT) (f). OilRedO staining of sections from liver (scale bars 200 μm) (g) and hepatic mRNA expression of FXR target genes (h). i, k Oxygen consumption (VO₂; in ml/(h*kg)) (i), heat (in kcal/(h*kg)) (j) and carbon dioxide production (VCO₂; in ml/(h*kg)) (k). l–o Relative mRNA expression of genes involved in thermogenesis and glucose uptake in BAT (l), H&E and UCP1 staining of sections from BAT (scale bars 200 μm) (m) as well as infrared images (n) and corresponding rectal body temperature (in °C) after 4 h of cold-exposure (o). Data are mean ± s.e.m; n = 5–10 animals per group with pooled data from 2 to 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001; unpaired two-tailed Student’s t test