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. 2019 Jul 26;2:276. doi: 10.1038/s42003-019-0521-4

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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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Fig. 1 — Tissue omega-6/omega-3 PUFA ratio influences the development of metabolic disorders and cancer. Wild type (WT) and FAT-2, FAT-1, and FAT-1+2 transgenic mice fed an identical Western diet for 16 months were subjected to several types of analyses at different time points. a Body weight at the age of 8 months. b Visceral white adipose tissue weight (g) after sacrificing the mice. c Nuclear magnetic resonance technique-based body composition analysis at the age of 16 months. Histopathological analysis (hematoxylin & eosin staining) of subcutaneous white adipose tissue (d) and inter-scapular brown adipose tissue (e) after sacrificing the mice. f Oral glucose tolerance test results obtained at the age of 8 months. g Fatty liver analysis performed on Oil Red O-stained liver specimens after sacrificing the mice. h Masson’s trichrome staining (red, keratin and muscle fibers; blue, collagen; light red or pink, cytoplasm and dark brown to black, cell nuclei) performed on liver specimens to estimate the extent of fibrosis. i Anatomical shape and gross appearance of the livers with tumors from the FAT-2 mice. j Differences in the incidence rate of liver cancer between wild type, FAT-2, FAT-1, and FAT-1+2 mice. Markers of metabolic endotoxemia [lipopolysaccharides (LPS) (k), LPS-binding protein (LBP) (l), soluble CD14 (m) and intestinal permeability (serum levels of FITC-dextran macromolecules) (n)] and chronic low-grade inflammation [tumor necrosis factor-α (TNF-α) (o), interleukin-6 (IL-6) (p), IL-1β (q), and monocyte chemoattractant protein 1 (MCP-1) (r)] measured at the age of 12 months. For c, n = 6 per group. For f, k–n and p–r, wild type (n = 7), FAT-2, FAT-1, and FAT-1+2 (n = 8 per group). For o, wild type (n = 7), FAT-2 and FAT-1 (n = 8 per group), FAT-1+2 (n = 7 per group). For others, wild type (n = 9), FAT-2, FAT-1 and FAT-1+2 (n = 10 per group). Data shown as mean ± standard error of mean. Data with different superscript letters are significantly different (P < 0.05) according to ordinary one-way (a–c, k–m, o–r) or repeated measures two-way ANOVA (f) or Kruskal–Wallis test (n) followed by Tukey’s or Dunn’s multiple comparisons test. ^*FAT-2 vs. FAT-1 and FAT-2 vs. FAT-1+2; ^&wild type vs. FAT-2; ^#wild type vs. FAT-1. Scale bar for images d and e: 1000 µm; g: 2000µm; h: 3000 µm