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Dietary cholesterol-oxidation products accumulate in serum and liver in apolipoprotein E-deficient mice, but do not accelerate atherosclerosis

Published online by Cambridge University Press:  09 March 2007

Miyuki Ando
Affiliation:
Laboratory of Nutrition Chemistry, Division of Bioresource and Bioenvironmental Sciences, Graduate School, Kyushu University, Fukuoka 812-8581, Japan
Hiroko Tomoyori
Affiliation:
Laboratory of Nutrition Chemistry, Division of Bioresource and Bioenvironmental Sciences, Graduate School, Kyushu University, Fukuoka 812-8581, Japan
Katsumi Imaizumi
Affiliation:
Laboratory of Nutrition Chemistry, Division of Bioresource and Bioenvironmental Sciences, Graduate School, Kyushu University, Fukuoka 812-8581, Japan
Corresponding
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Abstract

There are conflicting reports regarding the effect of dietary cholesterol-oxidation products (oxysterols) on the development of atherosclerosis in experimental animals. To address this issue, apolipoprotein (Apo) E-deficient mice were fed a purified diet (AIN-93) or the same purified diet containing 0·2 g cholesterol or 0·2 g oxysterols/kg. The dietary oxysterols had no significant effect on the serum lipid levels. Although all of the diet-derived oxysterols (cholest-5-en-3β,7α-diol, cholest-5-en-3β,7β-diol, cholestan-5α,6α-epoxy-3β-ol, cholestan-5β,6β-epoxy-3β-ol, cholestan-3β, 5α, 6β-triol, cholest-5-en-3β-ol-7-one and cholest-5-en-3β, 25-diol) accumulated in the serum and liver, only cholest-5-en-3β-ol-7-one and cholestan-3β, 5α, 6β-triol accumulated significantly (P<0·05) in the aorta. The oxysterol diet did not result in elevation of the aortic cholesterol level or the lesion volume in the aortic valve. These present results indicate that exogenous oxysterols do not promote the development of atherosclerosis in ApoE-deficient mice.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2002

References

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Dietary cholesterol-oxidation products accumulate in serum and liver in apolipoprotein E-deficient mice, but do not accelerate atherosclerosis
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