Figure 2
Intestinal lipid uptake and microbiota do not contribute to the iePPARγKO caloric restriction (CR) adipose tissue phenotype.
The relative mRNA expression levels of metabolism-associated genes and intestinal hormones were assayed by RT-qPCR in the intestinal epithelium of WT and iePPARγKO mice fed ad libitum or under CR (n = 10–12 mice) (a). Plasma concentrations of GIP, PYY and GLP-1 were measured for WT and iePPARγKO mice fed ad libitum and after CR (b); n = 7–9. WT CR mice and iePPARγKO CR mice were gavaged with oil, and their blood triglyceride (TG) concentrations measured at the indicated time points (n = 8 mice) (c). The energy content of faeces from WT CR and iePPARγKO CR mice was measured using direct calorimetry (n = 9 mice) (d). The relative mRNA expression levels of inflammatory factors and antibacterial and antiviral peptides were quantified in the intestinal epithelium of WT and iePPARγKO CR mice (n = 10–12 mice) (e). Murine faecal microbiota composition and metabolites were analysed by sequencing (f) and by NMR (g), and the two data sets jointly analysed (h). The statistical difference in plasma TG and faecal energy load was assessed by the Student’s t-test. Gene expression data were analysed using one-way ANOVA fallowed by Bonferroni post-hoc test. Symbols #, # #, and *, correspond to statistically significant differences between WT and WT CR data, KO and KO CR data, and WT CR and KO CR data, respectively. Error bars depict the standard error.
