Figure 4. LNK deficiency relieves hepatic steatosis. Representative images of pathologic specimen (A) of liver tissue were shown. Liver weight (B) was compared in WT or LNK-/- mice after HFD or NCD feeding for 16 weeks. Out-of-phase MRI for diagnosis of fatty liver of mice with HFD (C) and representative images of H&E staining of the liver (D, HFD: LNK-/- n=7, WT n=6; NCD: LNK-/- n=6, WT n=7. 10 images were quantified per mouse) were shown. Scale bars: 500 μm, 100 μm and 50 μm. Percentage of fat area in liver pathological tissue slice (E) and liver triglycerides (F) were shown. The mRNA expression of adipose differentiation-related molecule (G), lipolysis-related molecule (H), gluconeogenesis-related molecule (I), inflammation-related molecule (J) and endoplasmic reticulum stress-related molecule (K) in liver tissue of mice fed with HFD after 16 weeks were compared. HFD: LNK-/- n=7, WT n=6; NCD: LNK-/- n=6, WT n=7. Data were shown as mean ± SD. Statistical analysis was performed by ANOVA (B, C, E and F) and Student’s t-test (G to K). *p < 0.05, **p < 0.01, ***p < 0.001.