Figure 2.

Liver-specific deletion of CGI-58 exacerbates hepatic steatosis in male mice. (A) Representative images of H&E and Oil red O staining of the liver sections from the mice at necropsy. The Oil red O-stained area was quantified by ImageJ (n = 12 images per group). Three 20x images from each mouse liver section were taken under an Olympus miscroscope (n = 3 mice per group). (B,C) H&E staining of liver sections from the mice at necropsy. (D) Hepatic contents of triglycerides (TG), cholesterol, and phospholipids (PL) in the mice at necropsy (n = 6). The mass of cholesterol ester (CE) was calculated by multiplying the mass difference between total cholesterol (TC) and free cholesterol (FC) by 1.67. (E) Plasma concentrations of lipids in the male mice at necropsy (n = 5–6). (F) Immunoblots of hepatic proteins from the mice (n = 5–6 per group) fed the Western diet for 3 weeks. Immunoblots were quantified by densitometry. (G) Relative levels of hepatic mRNAs for genes involved in lipid synthesis and oxidation in the mice at necropsy (n = 4–5). GAPDH was used as an internal invariant control. SREBP-1c, sterol regulatory element binding protein-1c; ACC1, acetyl-CoA carboxylase 1; ME, malic enzyme; GPAT, mitochondrial glycerol-3-phosphate acyltransferase; DGAT2, acyl-CoA diacylglycerol acyltransferase 2; PPAR-α, peroxisome proliferator-activated receptor-alpha; CPT-1α, carnitine palmitoyltransferase-1alpha; ACO, acyl-CoA oxidase; LACD, long-chain acyl-CoA dehydrogenase. All samples were from the mice fed the Western diet, except those under (C), which were from the mice fed the chow. *P < 0.05; **P < 0.01.