Effect of dietary hyperlipidemic components and fish oil on concentration of lipids in liver and liver fatty acid profile of rats

This investigation was attempted to clarify the effects of dietary hyperlipidemic components and fish oil on concentration of lipids in liver and liver fatty acid profile of rats. In a first experiment male Sprague-Dawley rats were maintained on a semipurified low-fat diet with 6.5% coconut oil and 1.5% safflower oil, but without added cholesterol, or a high-fat hyperlipidemic diet supplemented with 7.3% coconut oil, 7.3% beef tallow, 0.4% safflower oil, and 1.5% cholesterol for 28 days. Rats fed the hyperlipidemic diet were then switched to fish oil diets with 1.4%, 2.8%, and 5.6% fish oil in exchange for coconut oil and beef tallow for, respectively, 10 and 20 days. In a second experiment male Sprague-Dawley rats were fed low-fat or high-fat diets without or with 1.5% added cholesterol for 28 days. Half of each group was then changed to a fish oil diet (for 20 days) which contained 5.6% fish oil in exchange for coconut oil and beef tallow. In experiment 1, rats fed the hyperlipidemic diet had enlarged fatty livers within 28 days. Experiment 2 showed that cholesterol in the diet was responsible for the accumulating liver lipids. Feeding diets with added cholesterol, the proportions of saturated fatty acids (SFA), especially 18:0, were markedly reduced in liver, whereas levels of monounsaturated fatty acids (MUFA) were greatly increased compared to diets without added cholesterol. This increase was most pronounced with respect to 16:1 and 18:1. In contrast, fish oil diets lowered MUFA level in liver in spite of its high MUFA content. Rats fed the highly saturated hyperlipidemic diet low in 18:2 n-6 had reduced 18:2 n-6 levels in liver compared to rats fed the low-fat diet without added cholesterol. Also, 20:4 n-6 level in liver was markedly reduced after the administration of the hyperlipidemic diet or the fish oil diets. Results of experiment 2 elucidate that cholesterol as well as fish oil sharply lowered 20:4 n-6 level in liver, which might be due to a reduced desaturation. In both experiments feeding fish oil increased all long-chain n-3 polyunsaturated fatty acids (PUFA) in liver. This occurred in a dose-dependent fashion and reached a maximum level with 5.6% fish oil in the diet. When additional cholesterol was applied 22:6 n-3 level in liver fell. This indicates also an impaired desaturation of PUFA due to dietary cholesterol.