Fig. 3: GPR81 ablation mitigates the tumour-induced wasting of muscle and adipose tissue.
From: Activation of GPR81 by lactate drives tumour-induced cachexia
a, Heat map illustrating the differential gene expression profiles of skeletal muscle of WT and GPR81 knockout (GPR81−/−) mice with or without subcutaneously xenograft LLC tumours (n = 3 for each group). b,c, Representative images of H&E staining (b) and grip strength (c) of skeletal muscle of WT control (n = 12), WT TB (n = 14), GPR81−/− control (n = 17) and GPR81−/− tumour-bearing (GPR81−/− TB, n = 14). Scale bars, 100 μm in b. d, Representative images of H&E staining of iWAT, gWAT and BAT. n = 5 for each group. Scale bars, 100 μm. e, Statistic results showing the distribution of adipocyte sizes in the iWAT and gWAT from WT and GPR81−/− mice with or without tumour (n = 5 for each group). f, Heat map illustrating the differential gene expression profiles of iWAT (n = 3 for each group). g, Relative mRNA levels of thermogenesis-related genes in the iWAT determined by quantitative PCR with reverse transcription (RT–qPCR; n = 8 for each group). h, Representative images and statistical results of immunofluorescence staining of UCP1 (red) in iWAT from WT and GPR81−/− with or without tumour (n = 4 for each group). Nuclei were stained with DAPI (blue). Scale bars, 100 μm. i,j, Serum NEFA (i) and glycerol (j) levels of WT and GPR81−/− mice with or without tumour (n = 9). All data are presented as the mean ± s.e.m. P values were determined by one-way ANOVA with Tukey’s multiple-comparisons test (c, g–j) or two-way ANOVA (e).
