SAA1/2 deficiency protects against hepatic steatosis. Male WT and SAA1/2−/− mice were fed a HFD for 16 weeks. (A) TG (left) and TCH (right) levels in the plasma of HFD-fed WT and SAA1/2−/− mice (n = 8). (B) NEFA levels in the plasma of HFD-fed WT and SAA1/2−/− mice (n = 8). (C) The liver weights of SAA1/2−/− mice and controls at 16 weeks post-HFD administration (n = 9). (D, E) Liver TG (D) and TCH (E) levels in WT and SAA1/2−/− mice (n = 9). (F) Representative images showing H&E staining (upper) and Oil Red O staining (bottom) of liver sections from WT and SAA1/2−/− mice that were fed a HFD for 16 weeks. Scale bar, 50 μm. (G) Quantifications of lipid droplet area in Oil Red O staining of representative liver sections (n = 5). (H) Plasma levels of ALT (left) and AST (right) in WT and SAA1/2−/− mice (n = 8). (I–K) mRNA levels of fatty acid synthesis (I), fatty acid uptake (J), and fatty acid β-oxidation (K) genes in the livers from WT and SAA1/2−/− mice (n = 9). All data are expressed as means ± SEMs. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)