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. 2020 Sep 17;10:15229. doi: 10.1038/s41598-020-71878-y

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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PSOn increases fatty acid oxidation in hepatocytes. Assessment of the mitochondrial function based on the oxygen consumption rate (OCR) in a time-course experiment is indicated for control (A) or stimulated (B) conditions. The endogenous (BSA alone) (C) and exogenous (Palmitate:BSA) (D) fatty acid oxidation was evaluated in basal or maximal conditions for control or PSOn-supplemented cells in the presence ( +) or absence (−) of etomoxir (eto) and plotted as the OCR. Bars indicate the mean ± SEM for each group (***p < 0.01; FCCP, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone).