title: Phytosterol oxidation products are absorbed in the intestinal lymphatics in rats but do not accelerate atherosclerosis in apolipoprotein E-deficient mice.
abstract: Phytosterol oxidation products (oxyphytosterols) are formed during the processing and storage of foods. However, it is unknown whether oxyphytosterols affect human health. To address these issues, we prepared beta-sitosterol and campesterol oxides, evaluated their lymphatic absorption in rats, and examined the effect of an oxyphytosterol diet on atherosclerosis in apolipoprotein (apo) E-deficient mice. The lymphatic absorption of cholesterol and 6 oxyphytosterols (7alpha-hydroxy, 7beta-hydroxy, beta-epoxy, alpha-epoxy, dihydroxy, and 7-keto) of beta-sitosterol or campesterol was assessed in thoracic duct-cannulated rats fed an AIN-93G-based diet containing 2.5 g of cholesterol, oxyphytosterols, or intact phytosterols per kg. Lymphatic recoveries (on a mass basis) of oxycampesterols (15.9 +/- 2.8%, n = 10) and oxysitosterols (9.12 +/- 1.77%, n = 10) were higher than for campesterol (5.47 +/- 1.02%, n = 12, P < 0.05) and beta-sitosterol (2.16 +/- 0.37%, n = 12, P < 0.05), but lower than for cholesterol (37.3 +/- 8.3%, n = 6, P < 0.05). Apo E-deficient mice were fed an AIN-93G-based diet containing 0.2 g oxyphytosterols or intact phytosterols per kg for 9 wk. Diet-derived oxyphytosterols accumulated in the serum, liver, and aorta. Furthermore, the oxyphytosterol diet increased oxycholesterol in the serum compared to the phytosterol diet. However, there was no significant difference between the 2 groups in the serum and aortic cholesterol concentration, the lesion area in the aortic root, or 8-iso-prostaglandin F2alpha concentration in the urine. These results indicate that exogenous oxyphytosterols are well-absorbed and accumulate in the body, but do not promote the development of atherosclerosis in apo E-deficient mice.
authors.affiliation: Laboratory of Nutrition Chemistry, Division of Bioresource and Bioenvironmental Sciences, Graduate School, Kyushu University, Fukuoka 812-8681, Japan.
authors.forename: Hiroko
authors.initials: H
authors.lastname: Tomoyori
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Kawata
authors.forename: Tomoko
authors.initials: T
authors.lastname: Higuchi
authors.forename: Ikuyo
authors.initials: I
authors.lastname: Ichi
authors.forename: Hiroyoshi
authors.initials: H
authors.lastname: Sato
authors.forename: Masao
authors.initials: M
authors.lastname: Sato
authors.forename: Ikuo
authors.initials: I
authors.lastname: Ikeda
authors.forename: Katsumi
authors.initials: K
authors.lastname: Imaizumi
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency*; D001161:Arteriosclerosis / Q000139:chemically induced*; D002784:Cholesterol / Q000031:analogs & derivatives* / Q000097:blood* / Q000493:pharmacokinetics / Q000494:pharmacology*; D007408:Intestinal Absorption / Q000187:drug effects; D008208:Lymphatic System / Q000378:metabolism; D008297:Male; D051379:Mice; D010084:Oxidation-Reduction; D010840:Phytosterols; D051381:Rats; D017207:Rats, Sprague-Dawley; D012855:Sitosterols / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D014018:Tissue Distribution
chemical_list: D001057:Apolipoproteins E; D010840:Phytosterols; D012855:Sitosterols; C021273:campesterol; D002784:Cholesterol