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. 2019 Mar 5;9:3535. doi: 10.1038/s41598-019-40419-7

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© The Author(s) 2019

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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The mitochondrial respiratory capacity in the EAT. (a) Representative graphs of mitochondrial respiratory capacity in the EAT in the non-coronary artery disease (non-CAD, n = 11) and CAD patients (n = 14). (b) The mitochondrial respiratory capacity at each state with non-fatty acid and fatty acid substrates in the EAT was lowered in the CAD group. Bar: mean ± SD. *P < 0.05. CI, complex I-linked substrates; CI + II, complex I + II-linked substrates; ETS, maximal electron transfer system capacity; FAO, fatty acid oxidation; LEAK, leak-state respiration (non-ADP stimulated respiration); OXPHOS, oxidative phosphorylation capacity (ADP-stimulated respiration).