Figure 3.

Exercise-trained mice have greater acylcarnitine metabolism, β-oxidation, respiration, and fatty acid uptake in the liver

Expression of genes (A) and proteins (B and C) involved in mitochondrial and AC metabolism and β-oxidation in the liver. Data are mean ± SEM (n = 6 per group), ∗p ≤ 0.05 One-way ANOVA. Red box on CACT indicates a well that was left blank and did not factor into the analysis.

(D) Bioenergetic profile of isolated hepatocytes from sedentary and exercise-trained mice and (E) basal OCR, ATP turnover, and maximal respiration in isolated hepatocytes. Data are mean ± SEM (n = 6, 3 replicates per group); ∗p ≤ 0.05 One-way ANOVA.

(F) Incubation of primary hepatocytes from sedentary or exercise-trained mice with BODIPY (fluorophore pentanoic acid) and within punctae (mitochondria), and etomoxir incubation.

(G) Quantification of fluorescent signal in primary hepatocytes/area mm². Data are mean ± SEM (n = 12 replicates per group); ∗p ≤ 0.05 vs. SED One-way ANOVA.

(H) Expression of genes in liver of sedentary and exercise-trained HFD-fed mice. Data are mean ± SEM (n = 6 per group), fold-change vs. SED; ∗p ≤ 0.05 One-way ANOVA.

(I) Model for exercise-training to increase pathways related to mitochondrial AC translocation, oxidation, and electron transport chain (ETC), resulting in enhanced hepatic mitochondrial function in high-fat fed mice.