Figure 5. Effects of AMP-activated protein kinase (AMPK) activation on lipid oxidation and mitochondrial function from mice on standard diet (STD), high-fat diet (HFD), and HFD + AICAR.

(a) Western blot analysis of the effect of HFD on phosphorylated acetyl-CoA carboxylase (ACQ in STD-, HFD-, and HFD +AlCAR-treated mice, (b) Relative densitometry of the immunoblot shows that phospho-ACC was reduced with HFD, whereas the AMPK activation prevented this inhibition. All figures were normalized with p-actin. Representative photomicrographs (original magnification ×400) illustrating phospho-ACC immunostaining in tubular epithelial cells in (c) STD, (d, e) HFD, and (f) HFD + AICAR. CD, collecting duct; G, glomerulus; PT, proximal tubule, (g) Quantitative analysis percent of phospho-ACC-positive staining area in mice on STD, HFD, or HFD + AICAR at 14 weeks. Values are means ± s.e.m. N = 6 in each group. Statistical analyses were performed by one-way analysis of variance (ANOVA) followed by Newman–Keuls, *P ≤0.05 versus mice on STD and ^#P ≤ 0.05 versus mice on HFD. (h–j) Cytochrome c oxidase (COX) activity, complex I activity, and citrate synthase measured in the kidney (respectively) in STD, HFD, and HFD + AICAR mice. Representative photomicrographs (original magnification ×400) illustrating COX staining in renal tissue of mice treated with (k) STD, (I) HFD, or (m) HFD + AIACAR. (n) Quantitative analysis of COX-positive staining. AICAR, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside.