Low amounts of trans 18 : 1 fatty acids elevate plasma triacylglycerols but not cholesterol and alter the cellular defence to oxidative stress in mice
Trans fatty acids are found mainly in processed foods. It has been shown that when their intake is high, total cholesterol, LDL-cholesterol and triacylglycerols are elevated, while HDL-cholesterol decreases. To evaluate a possible effect of these compounds, even in low amounts, C57Bl/6J mice were fe...
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Published in: | British journal of nutrition Vol. 94; no. 3; pp. 346 - 352 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Cambridge, UK
Cambridge University Press
01-09-2005
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Subjects: | |
Online Access: | Get full text |
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Summary: | Trans fatty acids are found mainly in processed foods. It has been shown that when their intake is high, total cholesterol, LDL-cholesterol and triacylglycerols are elevated, while HDL-cholesterol decreases. To evaluate a possible effect of these compounds, even in low amounts, C57Bl/6J mice were fed for 7 weeks a diet containing 13·6 % energy as partially hydrogenated rapeseed oil-enriched diet (Trans diet). The Trans diet contained 3 % energy as trans 18 : 1 fatty acid (elaidic acid). Control mice were on an isologous diet containing native rapeseed oil (Rapeseed diet) in which trans fatty acids were undetectable. Total, free and HDL-cholesterol as well as reverse cholesterol transport did not change. However, plasma triacylglycerol and VLDL levels increased. Hepatic gene expression in the Trans v. Rapeseed diet were compared using quantitative RT–PCR. The Trans diet produced a 2–3-fold elevation in mRNA of fatty acid synthase and microsomal transfer protein mRNA, explaining (at least in part) the observed increase in triacylglycerols and VLDL. In addition, mice on the Trans diet developed a deficiency in plasma vitamin E accompanied by a higher concentration of F2-isoprostanes, indicative of increased oxidative stress. The 78 kDa glucose-related protein (GRP78) mRNA expression increased 3–4-fold in liver, suggesting that a response against apoptosis was provoked by lipid peroxidation. |
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Bibliography: | PII:S0007114505001911 ArticleID:00191 ark:/67375/6GQ-LGL40PBL-Q istex:CB1920307D071FCE2BF86308AD12F0C6E3C28EFA ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0007-1145 1475-2662 |
DOI: | 10.1079/BJN20051512 |