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. 2024 Nov 15;14:28167. doi: 10.1038/s41598-024-78935-w

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 3 — Liver-specific knockout of MCU leads to an elevation in HFD-induced hepatic steatosis (n = 6). (A) Representative liver tissue photographs; Scale bar: 1 cm. (B) Liver weight-to-body weight ratio in different groups of mice. (C) Liver oil red O staining analysis images; Scale bar: 100 µm (40× objective). (D) Quantification of oil red O staining. (E) Hepatic triglyceride (TG) concentration. (F) Serum triglyceride concentration. (G) Representative liver H&E staining analysis images; Scale bar: 100 µm (40× objective). (H) Quantification of HE staining. All results are presented as means ± SD, with *p < 0.05/**p < 0.01 indicating statistical significance. Different letters meant there was significant difference among groups (p < 0.05).