Mechanism and therapeutic strategy of hepatic TM6SF2-deficient non-alcoholic fatty liver diseases via in vivo and in vitro experiments

Figure 2 Overexpression of TM6SF2 improves hepatic lipid accumulation in high-fat diet-induced mice models. A: Schematic representation of animal experiments. Mice were injected with AAV8-vector or AAV8-TM6SF2 virus via the tail vein and fed a high-fat diet for 16 wk (n = 5 mice per group); B: The efficiency of TM6SF2 overexpression in liver were shown; C-F: The liver/body weight ratio (C), the body weight (D), hepatic lipid content (E), and serum levels of alanine aminotransferase and aspartate transaminase (F) were shown; G: Representative images of gross morphology; H: Left, representative photos of fatty livers (top) and livers subjected to magnetic resonance imaging scanning (bottom) were shown. Right, the maximal cross-sectional area of livers is quantified by the number of pixels; I: Left, representative images of hematoxylin and eosin-staining (left) and Oil Red O-staining (right) of liver sections. Right, the nonalcoholic fatty liver disease activity score (left) and quantification of lipid (right, 8 fields of each mouse were examined) were performed. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. H&E: Hematoxylin and eosin; NCD: Normal chow diet; HFD: High-fat diet; NAS: Nonalcoholic fatty liver disease activity score.