Fig. 5

A deficiency in FFAR2 exacerbates the NAFLD/NASH phenotype. C57BL/6 WT or Ffar2^−/− mice were fed an HFC or an HFC + IN diet for 20 weeks. a Liver to body mass ratio (WT + HFC, n = 7; Ffar2^−/− + HFC, n = 8; WT + IN, n = 6, Ffar2^−/− + HFC, n = 6). b Plasma cholesterol (WT + HFC, n = 7; Ffar2^−/− + HFC, n = 8; WT + IN, n = 6, Ffar2^−/− + HFC, n = 6). c Liver cholesterol (WT + HFC, n = 7; Ffar2^−/− + HFC, n = 8; WT + IN, n = 7, Ffar2^−/− + HFC, n = 8). d Plasma ALT (WT + HFC, n = 7; Ffar2^−/− + HFC, n = 8; WT + IN, n = 7, Ffar2^−/− + HFC, n = 8). e Representative Masson’s trichrome staining of livers. Scale bar: 50 μm; black arrows show fibrosis, black arrowheads show hepatocyte ballooning. f Annotated gene ontology (GO) biological processes were assigned to genes upregulated in Ffar2^−/− mice versus WT mice in the liver after 20 weeks of consuming the HFC diet. Numbers next to bars represent the number of genes per pathway. g Heat maps of representative immune response- and fibrosis-related genes were constructed for genes differentially expressed in Ffar2^−/− mouse liver, as determined by RNA-seq. n = 3 per condition. Each point in a–f represents an individual mouse (thick bars, means; error bars, SEM). Data represent at least two independent experiments with similar results. *P < 0.05, **P < 0.01, ***P < 0.001 (ANOVA followed by post hoc Tukey’s test)