Dietary sitostanol reduces plaque formation but not lecithin cholesterol acyl transferase activity in rabbits.

The effects of graded amounts of dietary sitostanol (0.01, 0.2 and 0.8% (w/w)) were examined on plasma lipid-profile, coronary artery plaque development and lecithin:cholesterol acyl transferase activity in male New Zealand White rabbits given semi-purified diets for 10 weeks. All diets provided < 10% energy in the form of fat and contained 0.5% (w/w) cholesterol (C). Rabbits fed the semi-purified diet with 0.8% (w/w) (0.64 g/day) sitostanol had lower plasma total cholesterol (TC) (p = 0.006) (15.2 +/- 4.80 mmol/l) and very low-density lipoprotein-cholesterol (VLDL-C) (p = 0.007) (6.31 +/- 3.11 mmol/l) levels compared to the atherogenic control group (n = 6) (29.6 +/- 5.52 and 17.16 +/- 7.43 mmol/l, respectively). Dietary sitostanol at 0.8% (w/w) depressed plaque accretion in coronary arteries (p = 0.0014) and ascending aorta (p = 0.0004) compared with the atherogenic control, 0.01 and 0.2% (w/w) sitostanol-fed groups. No differences (p = 0.24) in the activity of lecithin:cholesterol acyl transferase (LCAT) were observed across groups, although plasma cholesterol fractional esterification rate was higher (p = 0.004) in the 0.8% (w/w) sitostanol fed animals compared with the atherogenic control. Significant negative correlations were demonstrated between sitostanol intake and plasma TC, LDL-C and VLDL-C levels. Hepatic campesterol levels were correlated (r = 0.3, p = 0.03) with plasma but not hepatic TC concentrations. These results demonstrate that dietary sitostanol at a concentration of 0.8% (w/w) or 0.64 g/day lowered plasma cholesterol levels and depressed atherosclerosis development in rabbits, but did not alter LCAT activity.