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. 2020 Jun 9;10:20. doi: 10.1038/s41387-020-0119-4

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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 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. 5 — Representative histopathological images of hematoxylin and eosin stained (top row) and oil-red-o stained (bottom row) hepatic tissue from rats fed a LED diet (left column), rats fed a HED for 4 weeks (middle column), and rats fed a HED for 26 weeks (right column), n = 3 for each group. H&E staining revealed an increase in distinct vacuoles in rats fed the HED diet (HED4 and HED26) compared to LED controls (LED26) (top row). Similarly, ORO staining showed that HED-fed animals exhibited more intensely red granules (HED4 and HED26) than LED controls (LED26) (bottom row). The quantitative scoring (Table) confirmed that hepatocellular lipidosis is apparent after consuming a HED diet for four weeks. We did not observe significant differences in the extent of hepatocellular lipidosis between the ST-HED (HED4) and LT-HED (HED26) groups. LED fed rats did not show signs of hepatocellular lipidosis. Graph represents mean ± SD binary analysis of the area fraction of ORO staining, which further confirms our results. Asterisk indicates statistical significance *P < 0.05.