Dietary fat saturation and hepatic acylcoenzyme A:cholesterol acyltransferase activity. Effect of n-3 polyunsaturated and long-chain saturated fat.

Abstract

The acylcoenzyme A:cholesterol acyltransferase (ACAT) activity in liver microsomes from rats fed a diet containing 14% menhaden oil (M p ) for 11 days was 117% higher than that in microsomes from rats fed a corresponding diet containing 14% cocoa butter (M s ). There were no differences in the cholesterol and phospholipid contents of M p and M s or in the activities of palmitoyl coenzyme A hydrolase and NADPH cytochrome c reductase. NADPH-dependent lipid peroxidation was higher in M p , whereas glucose 6-phosphatase activity was higher in M s . These findings indicate that the ACAT response to differences in dietary fat saturation is not due to a nonspecific effect of these diets on microsomal enzymes. When 1% cholesterol was added to the diets, the cholesterol content and ACAT activity of both microsomal preparations increased, but the ACAT activity of M p remained 60% higher than that of M s . Addition of cholesterol by incubation of the microsomes with liposomes also increased ACAT activity. At corresponding cholesterol contents, however, the ACAT activity of M p remained 50% to 70% above that of M s . There was no difference in the plasma cholesterol concentration in the two groups of rats, indicating that the ACAT effect probably is not due to a difference in the amount of circulating cholesterol available to the liver. M p contained 40% more polyunsaturated fatty acids and five times more n-3 polyunsaturates than M s . These findings suggest that the increase in ACAT activity in M p is due, at least in part, to the difference in the fatty acid composition of the microsomes. (Arteriosclerosis 3:242-248, May/June 1983)

Δ 6-desaturase activity in liver microsomes of rats fed diets enriched with cholesterol and/or ω3 fatty acids

“…Inclusion of 2 % cholesterol in the fish-oil diet, however, had no effect on A6desaturase activity or the C20 4,,,6-fatty-acid content of liver microsomes. It has been recently demonstrated that the rate ofcholesterol ester formation by liver microsomal acyl-CoA: cholesterol acyltransferase is accelerated by supplementing the rat diet with fish oil (rich in C20:5 and C22:6,.3 fatty acids) [38,39]. This would mean that C20:50:,3 and/or C22:60,3 fatty acids, instead of C20:4,.6 fatty acid, are utilized for cholesterol esterification in animals fed on a fish-oil-supplemented diet and that C20:5,,.3 and C22:6,.3 fatty acids are readily available for increased demand in utilization caused by 2 % cholesterol.…”

Effect of Olive Oil-Fried Sardine Consumption on Liver Lipid Composition and Fatty Acid Cholesterol Esterification in Hypercholesterolemic Rats

“…A menhaden oil containing more than 17% of PUFA n-3 produced lower liver cholesterol content than oleic acid (Mohamed et al, 2002). Several authors have found the enzyme acyl-CoA : cholesterol acyltransferase (ACAT) is stimulated by diets enriched with PUFA n-3, a situation that in turn explains the increase of cholesterol ester pool found for several authors in this organ (Spector et al, 1980;Johnson et al, 1983;Field et al, 1987;Parks and Bullock, 1987). However, in all these studies the effects of PUFA n-3 Table 3.…”