Trans fatty acids (TFA) from industrial sources [i.e. partially hydrogenated vegetable oil (PHVO)] have been associated with several chronic human diseases, especially coronary heart disease (CHD). The possible contribution of individual TFA to overall CHD risk remains largely unknown. The objective of the present study was to investigate the effects of 2 major trans 18:1 isomers, trans-9 18:1 [elaidic acid (EA)] and trans-11 18:1 [vaccenic acid (VA)] on plasma lipid biomarkers of CHD risk. Thirty-two male Golden Syrian hamsters were randomly assigned to 1 of 4 dietary treatments: 1) control "Western" diet; 2) PHVO supplement; 3) EA supplement; and 4) VA supplement. Fat supplements were incorporated into the respective treatment diets at 2.5 g/100 g of diet. Compared with the control diet, the PHVO diet increased the plasma ratios of total:HDL-cholesterol and nonHDL:HDL-cholesterol by 17 and 23%, respectively. In contrast, these values decreased by 27 and 46% after the EA treatment and 8 and 14% after the VA treatment, respectively, indicating an improvement (reduction) in CHD risk. With regard to liver lipids, the EA diet reduced the content of (n-3) and (n-6) PUFA relative to the other treatments, suggesting an inhibition of enzymes common to the 2 biosynthesis pathways. Overall, results demonstrate that the hypercholesterolemic effects of PHVO are not dependent on the presence of EA or VA and that other bioactive components in PHVO must be responsible for its associated adverse health effects.

Reduction of stearoyl CoA desaturase (SCD) activity has been shown to induce resistance to diet-induced obesity in mice. In the present study, SCD was inhibited by feeding sterculic oil (SO) to male Golden Syrian Hamsters fed high-fat diets with or without added dietary cholesterol. In the absence of cholesterol, SO had little impact on adipose tissue mass or plasma lipoprotein concentrations. When cholesterol was included in the diet, inhibition of SCD resulted in reduced body weight, adipose tissue mass, and feed efficiency. These animals also exhibited a marked hypercholesterolemia, with an accumulation of free-cholesterolrich particles within the LDL density range, and reduced hepatic cholesterol esterification. This was accompanied by a 20-fold increase in plasma alanine aminotransferase, which was suggestive of significant hepatic damage. Hepatic acetyl CoA carboxylase and fatty acid synthase mRNA concentrations were reduced by feeding cholesterol and SO, whereas lipoprotein lipase and SCD mRNA were increased. These changes were associated with decreased hepatic sterol regulatory element binding protein 1a and 1c mRNA concentrations. Thus, inhibition of SCD activity in the cholesterol-fed hamster results in a reduction in overall body weight and adipose tissue deposition. However, this also causes marked hypercholesterolemia and potential liver

Stearoyl-CoA desaturase (SCD) introduces a double bond at the D9 position of various fatty acids. The enzyme's primary function appears to be the conversion of stearic acid to oleic acid (cis-9 18 :1), the predominant MUFA in the body. Reduction of SCD activity has been shown to result in reduction of body fat in mice, whereas, increased SCD levels have been found to be increased in obese mouse models (1). The Golden Syrian hamster has been shown to exhibit a number of advantages compared with other small-animal models of lipid and lipoprotein metabolism. While four isoforms of SCD have been reported in mice (each of which show specific tissue expression and response to nutritional factors), until recently only one isoform had been described in the hamster. However, a recent report has suggested that this species expresses at least three isoforms analogous to SCD1, SCD2 and SCD3 of the mouse (2). The present experiment has investigated the effects of dietary fat and cholesterol (chol) on the expression and abundance of the three SCD isoforms in hamster liver and white adipose tissue. Male Golden Syrian hamsters (eight per group) were fed a low-fat chow-based diet (chow) alone or with 0.2% (w/w) chol or 15 % (w/w) added fat (formulated to represent the fatty acid composition of a typical Western diet) or both. The diets were fed for 4 weeks, after which the animals were killed and the liver and adipose tissues were removed, snap-frozen in liquid N 2 and stored at-80 C until required for determination of mRNA concentration. The steady-state mRNA concentration for all three SCD isoforms and TATA boxbinding protein was determined by real-time PCR. The abundance was calculated using the formula: abundance = efficiency-Dct(2). Data were analysed by two-way ANOVA, exploring significant effects of chol, fat or an interaction between the two (chol • fat). SCD1 was the major isoform expressed in both liver and adipose tissue, with its expression in the liver being approximately 50-fold higher than SCD3 and 300-fold higher than SCD2. Diet had little impact on the expression of any of the isoforms in adipose tissue. However, specific effects of diet were seen on the relative abundance (arbitrary units) of each of the isomers in the liver (Table).