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Conjugated and non-conjugated octadecaenoic acids affect differently intestinal acyl coenzyme A: Cholesterol acyltransferase activity

Abstract We investigated the relative hypocholesterolemic activity of linoleic acid (LA), conjugated linoleic acid (CLA), α-linolenic acid (LN) and conjugated linolenic acid (CLN) in hamsters. Five groups of hamsters ( n = 10 each) were fed either the control diet or one of the four fatty acids-supp...

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Published in:Atherosclerosis 2008-05, Vol.198 (1), p.85-93
Main Authors: Lam, Cheuk Kai, Chen, Jingnan, Cao, Ying, Yang, Lin, Wong, Yin Mei, Yeung, Sai Ying Venus, Yao, Xiaoqiang, Huang, Yu, Chen, Zhen-Yu
Format: Article
Language:English
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Summary:Abstract We investigated the relative hypocholesterolemic activity of linoleic acid (LA), conjugated linoleic acid (CLA), α-linolenic acid (LN) and conjugated linolenic acid (CLN) in hamsters. Five groups of hamsters ( n = 10 each) were fed either the control diet or one of the four fatty acids-supplemented diets for 6 weeks. Results demonstrated that the four octadecaenoic acids decreased plasma cholesterol differently, with CLA being the most effective. Western blotting and RT-PCR analysis demonstrated that the four octadecaenoic acids had no effect on sterol regulatory element binding protein-2 (SREBP-2), liver X receptor (LXR), 3-hydroxy-3-methylglutary-CoA reductase (HMGR), LDL receptor (LDLR), and cholesterol-7α-hydroxylase (CYP7A1). However, the four octadecaenoic acids increased the excretion of fecal neutral sterols with CLA being most effective followed by LN, LA and CLN, suggesting they all differentially affect cholesterol absorption. Dietary CLA was associated with the least intestinal acyl coenzyme A: cholesterol acyltransferase (ACAT) activity followed by LN, LA and CLN in a decreasing trend. Since esterification of cholesterol is catalyzed by intestinal ACAT, and is a rate-limiting step in cholesterol absorption, it was concluded that the varying effects of CLA, LN, LA and CLN on blood cholesterol were mediated, at least in part, by their inhibition on intestinal ACAT activity.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2007.11.001