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. 2020 Dec 17;62:100013. doi: 10.1194/jlr.RA120000737

Fig. 6.

Fig. 6

Mechanisms involved in hepatic steatosis progression in Lpcat3KOMac mice when fed a high-fat diet for 16 weeks. A, B: F4/80 staining in histological sections of adipose tissue and liver of Ctrl and Lpcat3 KOMac (n = 7 vs. 13, respectively). C: Liver mRNA levels of inflammatory genes of wild-type and Lpcat3KOMac mice (n = 7 vs. 13, respectively). D: Relative Lpcat3 mRNA levels of in isolated Kupffer cells (n = 3 in each group). E: Relative content of fatty acid at the sn-2 position of pPE from isolated Kupffer cells after HFD. Data are expressed as a % of total pPE and are normalized as 1 in the WT group (n = 3 in each group). F: Volcano plot of differentially expressed genes in Kupffer cells at the end of the diet (n = 3 in each group). G: Eicosanoid content in the liver of WT and Lpcat3KOMac mice (n = 7 vs. 13, respectively). H: Relative mRNA levels of genes involved in Cytochrome P450 pathway in the whole liver (n = 4 in each group). Data are expressed as mean + SEM (∗P < 0.05 vs. WT Mann-Whitney test).