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Labeled cholesterol and its esters were injected via the portal vein into bile duct‐cannulated rats, subsequent to a 7 week regimen of either 5% safflower oil or 5% beef tallow in a hypercholesterolemic diet. Analysis of bile collected over a 6 hr period from the safflower group showed 8.6% higher output of bile acids, 13.6% higher conversion of3H‐cholesterol to bile acids and 40% higher conversion of [4‐14C]cholesteryl oleate to bile acids than bile collected from the tallow group. During the 1st hr conversion of both oleyl and linoleyl esters of14C‐cholesterol to bile acids was much slower than conversion of the free3H‐cholesterol to bile acids, thus eliminating these esters as preferred substrate for bile acid formation. However at 6 hr two‐thirds of the injected14C of oleyl ester was recovered in the liver, and about half of this was in the form of free cholesterol. Thus cholesterol ester hydrolase, though inhibited by dietary cholesterol, evidently did not impose limitations on formation of free cholesterol for subsequent oxidation reactions. Specific radioactivities were of doubtful significance because of uncertainities as to “active” pool size. The data suggest that dietary linoleate exerts its hypocholesterolemic effect in some manner other than ester formation and that its point of action involves stimulation of cholesterol oxidation to bile acids.
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McGovern et al. (1973) studied this question.
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