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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Kidney Int. 2013 Dec 4;85(3):611–623. doi: 10.1038/ki.2013.462

Figure 3. Effects of AMP-activated protein kinase (AMPK) activation on tubular histology from mice on standard diet (STD), high-fat diet (HFD), and HFD + AICAR.

Figure 3

Representative photomicrographs (original magnification ×400) illustrating vacuolated proximal convoluted tubular cells (*) and loss of brush border (arrow) in (a) STD, (b) HFD, and (c) HFD + AICAR mice. Representative photomicrographs (original magnification ×1000) illustrating vacuolated proximal convoluted tubular cells (*) and impaired brush border (arrow) in (d–f) HFD mice. (g) Quantitative analysis of number of vacuolated tubules per mm2. Representative photomicrographs (original magnification ×400) illustrating nitrotyrosine staining in tubular epithelial cells in (h) STD, (i, j) HFD, and (k) HFD + AICAR. (I) Western blot analysis of the effect of HFD on NADPH oxidase 4 (NOX4) expression in STD-, HFD-, and HFD +AlCAR-treated mice, (m) Relative densitometry of the immunoblot shows that NOX4 was upregulated with HFD, whereas the AMPK activation prevented this rise. 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. AICAR, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside.