Fig. 2: GRAIL deficiency attenuates high-fat diet (HFD)-induced hepatic steatosis and obesity.

A, B Histological images of liver tissues after Grail staining in the indicated groups. C Wild-type (WT) and GRAIL knockout (KO) mice were fed normal chow diet (ND) (n = 5) or HFD (n = 5) for 8 weeks, and their body weights were determined. D, E Liver weight (n = 5) and Liver to body weight ratio (n = 5) of the WT and GRAIL KO mice after an 8-week ND or HFD treatment. F–I Analysis of serum triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the indicated groups after ND or HFD treatment (n = 5/group). J–M Histological images of liver tissues after hematoxylin and eosin (HE) staining and oil red O staining in the indicated groups. N The mRNA expressions of genes related to cholesterol synthesis and efflux and fatty acid uptake, synthesis, and beta-oxidation in the liver samples of WT and GRAIL KO mice after ND or HFD treatment (n = 5–6/group), determined using real-time quantitative polymerase chain reaction (RT-qPCR). The data are presented as mean ± standard deviation (SD). O Fatty acid synthase (FASN), CD36, and sterol regulatory element-binding protein 1c (SREBP-1c) (mature form) in liver samples of WT and GRAIL KO mice fed with ND or HFD were detected with immunoblotting. One-way ANOVA with Newman-Keuls post hoc test or Student’s t-test are used to evaluate the statistical significance. *P < 0.05; **P < 0.01; ***P < 0.001.