Experimental atherosclerosis in rabbits fed cholesterol-free diets: Influence of chow components

Abstract

It has been shown that addition of saturated fat to a semi-synthetic ration is atherogenic for rabbits, whereas addition of the same amount of fat to rabbit chow has no effect. To test the factor in the chow which may exert this "protective" action, we fed rabbits the following diets: (SS): semi-synthetic containing 14% hydrogenated coconut oil; (SS-PF): semi-synthetic containing 12% hydrogenated coconut oil (HCNO) and 2 % of the fat extracted from rabbit chow; (XP-HCNO): the fat-extracted chow residue plus 14 % HCNO; and (PC-HCNO): chow milled with additional 12 % HCNO. Another group of rabbits was fed the semi-synthetic diet augmented with 1 % lauric acid (SS-LA) to ascertain if the atherogenicity of free fatty acids would be evident in a semi-synthetic diet as it has been in rabbits fed cholesterol. One chow-fed group of rabbits (PC) served as control. After 6 months of feeding it was found that all the groups of rabbits fed diets containing HCNO had elevated liver cholesterol levels and elevated liver ester cholesterol. The groups fed the semi-synthetic diet (SS, SS-PF and SS-LA) had elevated serum cholesterol levels (200-250 mg/100 ml), elevated serum β-lipoprotein cholesterol levels and cho-lesterol/phospholipid ratios greater than 1.00. They all exhibited marked atherosclerosis. Group XP-HCNO had moderately elevated serum cholesterol levels (64 mg/ 100 ml as compared to 40 mg/100 ml in the normal rabbits), elevated serum ^-lipoprotein cholesterol and a C/PL of 1.21, but atheromata in this group were minimal. The group fed chow and 12% HCNO (PC-HCNO) exhibited no abnormalities in its serum lipid spectrum and no atheromata. The data suggest that the complete chow is required to overcome the effects of HCNO on serum lipids, but the extracted chow residue will inhibit aortic atherosclerosis, at least over a 6-month feeding period. The pattern of liver and serum lipids suggest that in animals fed HCNO there is an initial increase in liver cholesterol, followed by increases in serum total and β-lipoprotein cholesterol, and then by aortic plaque formation. Cholesterol biosynthesis from [l-14C]acetate was inhibited in most of the groups fed HCNO, eliminating in- creased cholesterogenesis as a mechanism for the moderate hypercholesteremia which we observed.