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. 2019 Mar 6;9:3656. doi: 10.1038/s41598-019-40153-0

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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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Genome-wide linkage mapping of liver histopathology identifies QTLs for NAFLD on mouse chromosome 18. Linkage mapping data and allele effects are shown for the grades of macrovesicular lesions (A,D) microvesicular lesions (B,E) and inflammation (C,F) in high fat diet (HFD) fed F2 mice. LOD scores are plotted against map distances (centimorgans) across the genome (A–C) and on chromosome 18 (D–F). Horizontal red lines indicates statistically significant LOD thresholds (P = 0.001). Effects of genotypes at marker locus rs13483370 on chromosome 18 exhibiting the strongest evidence of linkage to macrovesicular steatosis (G), microvesicular steatosis (H) and inflammation (I) are illustrated by mean values (±SD) of the phenotypes calculated according to the genotype homozygous for the 129S6 or BALB/c alleles, or heterozygous at the locus. Typical examples of liver histopathology in HFD-fed F2 mice homozygous at marker locus rs13483370 for the BALB/c (J) or the 129S6 (K,L) allele are shown (Magnification x50).