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. 2019 Jul 17;3(8):1036–1049. doi: 10.1002/hep4.1381

Figure 4.

Figure 4

GLKO mice do not develop fibrosis under conditions of an HFD. All the bar graphs represent mean ± SEM. (A) Sirius red staining of livers of HFD‐treated WT and GLKO mice. Perisinusoidal focal fibrosis shown by arrows. (B) mRNA levels of markers of fibrosis were examined by qRT‐PCR, *P < 0.05 WT ND versus WT HFD; #P < 0.05 GLKO ND versus GLKO HFD; €P < 0.05 WT HFD versus GLKO HFD. (C) Inhibitors of proliferation and key regulators of liver biology C/EBPα, CUGBP1, HNF4α, Rb, and p53 are increased in HFD‐treated GLKO mice. Protein levels of C/EBPα, ph‐S193‐ C/EBPα, CUGBP1, HNF4α, Rb, Rb‐S780‐ph, p53, and MDM2 were determined in nuclear extracts isolated from livers of HFD‐treated GLKO mice by western blotting. For Gank IP, Gank was immunoprecipitated and levels of C/EBPα, CUGBP1, HNF4α, Rb, and p53 were determined from these immunoprecipitations. (D) Protein levels C/EBPα, CUGBP1, HNF4α, Rb, ph‐Rb, and p53 were calculated as ratios to β‐actin, *P < 0.05 WT ND versus WT HFD; #P < 0.05 GLKO ND versus GLKO HFD; €P < 0.05 WT HFD versus GLKO HFD. (E) Hypothesis for the molecular basis of the improvements of health in GLKO mice treated with an HFD. Abbreviations: CRM, Cross reactive molecule; tot, total; UP, up‐regulated.