Fig. 4. Chronic clenbuterol treatment decreases fatty acid oxidation in SKM in vivo.

Prior to metabolomics and gene expression studies, lean WT mice consumed drinking water containing clenbuterol (30 mg/l; clenb. H₂O) or regular drinking water (reg. H₂O) for 5 days. All studies were carried out with male mice that were ~12 weeks old. a Graphic representation of differentially expressed genes within the fatty acid oxidation pathway in SKM (quadriceps muscle) of clenb. H₂O vs. reg. H₂O mice (n = 5/group). b–e Changes in the levels of SKM transcripts involved in fatty acid (FA) uptake (b), lipolysis (c), import of FAs into mitochondria (d), and FA β-oxidation (e). SKM gene expression levels (RPKM) were determined via RNA-Seq in fasted (15 h) and freely fed WT mice by using the Genomatix Genome Analyzer platform. Data are presented as means ± SEM. ^#Significantly regulated (two-tailed Wald test (DESeq2)) (n = 5/group, adjusted p-value < 0.05). f Fold changes (clenb. vs. reg. H₂O) of acylcarnitine levels in SKM of fasted (15 h) WT mice, determined by high-throughput metabolomics (n = 7/group). The red bars indicate significant clenbuterol effects (ANOVA contrast). RPKM, reads per kilobase of transcript per million of mapped reads. Source data are provided as a Source data file.