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.
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School of Dietetics and Human Nutrition, McGill University, Macdonald Campus, Ste-Anne-de-Bellevue, Quebec, Canada.
Jones
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PJ
Frohlich
J J
JJ
D000818:Animals; D000924:Anticholesteremic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D001161:Arteriosclerosis / Q000378:metabolism / Q000473:pathology*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects / Q000201:enzymology / Q000473:pathology*; D004032:Diet; D004951:Esterification; D008297:Male; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000378:metabolism*; D010840:Phytosterols / Q000494:pharmacology; D011817:Rabbits; D012855:Sitosterols / Q000008:administration & dosage* / Q000494:pharmacology
D000924:Anticholesteremic Agents; D010840:Phytosterols; D012855:Sitosterols; D002784:Cholesterol; C021255:stigmastanol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase