British Journal of Nutrition

Research Article

Low amounts of trans 18 : 1 fatty acids elevate plasma triacylglycerols but not cholesterol and alter the cellular defence to oxidative stress in mice

Nadège Cassagnoa1, Antonio Palos-Pintoa1, Pierre Costeta2, Dominique Breilha3, Michel Darmona1 and Annie M. Bérarda1 c1

a1 Laboratoire de Biochimie et de Biologie Moléculaire, EA no 3670, Centre Hospitalier Universitaire de Bordeaux, Université Victor Ségalen Bordeaux 2, 146 rue Léo-Saignat, 33076 Bordeaux, France

a2 Animalerie Transgénique, Université Victor Ségalen Bordeaux 2, 146 rue Léo-Saignat, 33076 Bordeaux, France

a3 Pharmacie Hospitalière, Hôpital Haut-Lévêque, 33604 Pessac, France

Abstract

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.

(Received September 23 2004)

(Revised March 15 2005)

(Accepted April 21 2005)

Correspondence:

c1 *Corresponding author: Dr Annie M. Bérard, email annie.berard@u-bordeaux2.fr

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