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. 2017 Sep 8;8:494. doi: 10.1038/s41467-017-00664-8

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Mitochondrial morphological and functional aberrations in HFD-CKO hearts. a The content of mtDNA was measured by the ratio of Cox1 to cyclophilin A. b Mitochondria was examined by TEM (×1400). Representative images showing reduced and disorganized mitochondria cluttering in the cytosol of HFD-CKO hearts (scale bar: 2 µm). The quantitative analysis of mitochondria number is provided in bar graphs. c Higher magnification (×4800) of TEM images show disarrayed cristae, vacuoles and a reduced electron density of the matrix in the HFD-CKO mitochondria (scale bar: 0.5 µm), M symbolize mitochondria, arrows indicate lipid droplets. Quantitative analysis of cristae area, disorganized cristae in mitochondria, lipid droplet number, respectively, is provided in the bar graphs (n = 6 mice per group). d Respiratory rates of mitochondrial ETC complexes were measured in saponin-permeabilized myocardial fibers. With glutamate/malate as substrates, complex I respiratory rate was found to be decreased in HFD-CKO hearts. e Significantly reduced ATP production in HFD-CKO hearts was determined. Consistent with this, the respiratory control ratio (RCR) was lower in HFD-CKO hearts. f Analysis of complex I in mitochondria homogenates using palmitoylcarnitine as a substrate showed that ERK5-deficient mitochondria of HFD-fed mice had a reduction in FA-driven respiration. g Mitochondrial fuel oxidation was suppressed in HFD-CKO hearts evidenced by activity measurement of β-hydroxylacyl CoA dehydrogenase and pyruvate dehydrogenase (Pdh) (n = 7 mice per group). Data are presented as means ± SD