Dietary n-3 fatty acids promote arrhythmias during acute regional myocardial ischemia in isolated pig hearts.

OBJECTIVE: Dietary supplementation with fish oil-derived n-3 fatty acids reduces mortality in patients with myocardial infarction, but may have adverse effects in angina patients. The underlying electrophysiologic mechanisms are poorly understood. We studied the arrhythmias and the electrophysiologic changes during regional ischemia in hearts from pigs fed a diet rich in fish oil. METHODS: Pigs received diets rich in fish oil, in sunflower oil, or a control diet for 8 weeks. Hearts were isolated and perfused. Ischemia was created by occluding the left anterior descending artery. Diastolic stimulation threshold, refractory period, conduction velocity, activation recovery intervals and the maximum downstroke velocity of 176 electrograms were measured in the ischemic zone. Spontaneous arrhythmias during 75 min of regional ischemia were counted. RESULTS: More episodes of spontaneous ischemia-induced sustained ventricular tachycardia and ventricular fibrillation occurred in the fish oil and sunflower oil group than in the control group. More inexcitable myocardium was present in the ischemic zone in the group fed fish oil or sunflower oil than in the control group after 20 min of ischemia. After 40 min of ischemia, more block occurred in the control group than in the other groups. The downstroke velocity of the electrograms in the ischemic border zone was lower in the fish oil group and sunflower oil group than in the control after 20 min. CONCLUSIONS: A diet rich in fish oil results in proarrhythmia compared to a control diet during regional ischemia in pigs. Myocardial excitability is reduced in the fish oil and sunflower oil group during the early phase of arrhythmogenesis. In the late phase of arrhythmogenesis, excitability is more reduced in the control group than in the fish oil and sunflower oil group.

Prolonged feeding of mice with conjugated linoleic acid increases hepatic fatty acid synthesis relative to oxidation.

Feeding mice conjugated linoleic acid (9 cis,11 trans/9 trans,11 cis-and 10 trans,12 cis-CLA in equal amounts) resulted in triacylglycerol accumulation in the liver. The objective of this study was to examine whether this steatosis is associated with changes in hepatic fatty acid synthesis and oxidation. Therefore, we measured the activities of key enzymes of fatty acid synthesis, i.e., acetyl-CoA carboxylase and fatty acid synthase and of fatty acid oxidation, i.e., 3-hydroxy-acyl-CoA dehydrogenase and citrate synthase in livers of mice fed a diet with 0.5% (w/w) CLA. CLA (a 1:1 mixture of the 10 trans, 12 cis and 9 cis, 11 trans isomers of octadecadenoic acid) was administered for 3 and 12 weeks with high-oleic sunflower oil fed as control. The proportion of body fat was significantly lower on the CLA than on the control diet and this effect was already significant after 3 weeks. The specific activites of 3-hydroxy-acyl-CoA dehydrogenase and citrate synthase were unaffected by CLA both after 3 and 12 weeks. The specific activity of fatty acid synthase was nonsignificantly raised (by 12%) after 3 weeks on the CLA diet but had increased significantly (by 34%) after 12 weeks of feeding. The specific activity of acetyl-CoA carboxylase had also increased both after 3 weeks (by 53%) and 12 weeks (by 23%) on the CLA diet, but this effect did not reach statistical significance. Due to CLA-induced hepatomegaly, the overall capacity for both fatty acid oxidation and synthesis-as evidenced by the total hepatic activities of 3-hydroxy-acyl-CoA dehydrogenase, citrate synthase, acetyl-CoA carboxylase, and fatty acid synthase-was significantly greater in the CLA-fed group after 12 weeks, although the overall capacity for fatty acid synthesis had increased more than that for fatty acid oxidation. Thus, this study indicates that prolonged, but not short-term, feeding mice with CLA increased hepatic fatty acid synthesis relative to oxidation, despite the decrease in body fat and the increase in liver weight seen earlier. It is concluded that the observed CLA-induced changes in hepatic fatty acid synthesis and oxidation are the result, rather than the cause, of the lowering of body fat.

Thermally oxidised sunflower-seed oil increases liver and serum peroxidation and modifies lipoprotein composition in rats.

Peroxidation of LDL and other lipoproteins is thought to play a central role in atherogenesis. Dietary thermally oxidised oils may increase atherogenic risk in consumers by increasing their oxidative status. The present paper compares the effects of two diets containing unused sunflower-seed oil (US) or sunflower-seed oil repeatedly used in frying (FS) (both 15 g/100 g diet) on weight gain, food efficiency ratio, serum lipid levels and lipoprotein composition, and the content of thiobarbituric acid-reactive substances (TBARS) in the liver, serum, and lipoproteins in growing Wistar rats. After sixty potato fryings the FS contained 27.7 g polar material/100 g oil and 16.6 g oligomers/100 g oil. The FS-fed rats had a significantly lower weight gain and food efficiency ratio. Liver-TBARS increased due to the consumption of the highly altered oil and showed a significant linear relationship (all r > 0.68; P < 0.002) with the ingestion of thermally oxidised compounds. Serum-, VLDL-, LDL- and HDL-TBARS were significantly higher in the FS-fed rats (all P < 0.001). Concentrations of serum total and non-esterified cholesterol and phospholipids were significantly higher in the FS-fed rats (P < 0.05, P < 0.05, and P < 0.001, respectively). Serum triacylglycerol concentrations did not vary between the two dietary groups. Total and esterified cholesterol and phospholipid levels increased significantly in the HDL fraction (P < 0.05, P < 0.05, and P < 0.001, respectively) of the FS-fed rats. HDL-cholesterol and HDL-phospholipids were significantly correlated with liver-TBARS (r > 0.747; P < 0.0001), VLDL-TBARS (r > 0.642; P < 0.003), LDL-TBARS (r > 0.475; P < 0.04), and HDL-TBARS (r > 0.787; P < 0.0001). The data suggest that the rat increases HDL as a protecting mechanism against the peroxidative stress induced by the consumption of a diet containing the thermally oxidised oil.

Effect of conjugated linoleic acid on body composition and plasma lipids in humans: an overview of the literature.

Studies in mice have indicated that feeding diets containing 0.5-1% conjugated linoleic acid (CLA) considerably reduces body fat. These findings have attracted much interest because of the potential use of CLA as a tool to promote weight loss in humans. Several CLA studies in humans have now been published, and the objective of the present review was to give an overview of these experiments. Most of the studies were done in free-living subjects and were not strictly controlled for nutrient and energy intakes. None of the studies found a significant reduction in body weight, and only 2 studies showed a significant but relatively small body fat-lowering effect. Some studies suggested that CLA may have a tendency to increase lean body mass. Furthermore, there are indications from animal studies that CLA may have effects on plasma lipids. However, only one study in humans showed a significant HDL-cholesterol-lowering effect of CLA; in all the other studies, there were no significant effects on plasma total, LDL-, and HDL-cholesterol concentrations or on plasma triacylglycerol concentrations. Thus, the results of the studies in humans indicate that the effect of CLA on body fat is considerably less than that anticipated from mice studies and that CLA has no major effect on plasma lipids.