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. 2008 Apr 18;283(16):10522–10534. doi: 10.1074/jbc.M707659200

FIGURE 6.

FIGURE 6.

Depletion of hepatic ACAT2 results in augmented free cholesterol and phospholipid secretion during isolated liver perfusion. Male LDLr-/-, apoB100-only mice were fed a low-fat (20% of energy as fat), moderate cholesterol (0.1%, w/w) diet for 8 weeks (A and B) or 14–16 weeks (C) in conjunction with biweekly injections (25 mg/kg) of a non-targeting ASO (control ASO) or an ASO targeting the knockdown of ACAT2 (ACAT2 ASO). Mice with targeted gene deletion of ACAT2 were treated with saline for 8 weeks as a total body knock-out control (ACAT2-/-). Thereafter, isolated liver perfusions were carried out to determine the mass accumulation rates of TG, TC, CE, FC, and PL. Data in panel A represent the mean ± S.E. from 5 control ASO-treated mice, 5 ACAT2 ASO-treated mice, and 4 ACAT2-/- mice; asterisk, significantly different from the control ASO group within each lipid classification (p < 0.05). Panel B represents Western blot confirmation that ACAT2 protein was not detectable in the ACAT2 ASO-treated or ACAT2-/- livers used for perfusion following 8 weeks of treatment. NS, nonspecific background band that serves as a loading control. Panel C represents a subset of mice that were chronically (14–16 weeks) treated with ASOs. Lipid accumulation rates in panel C were determined by gas-liquid chromatography.