Turnover of bile acids in the hypercholesterolemic rat as influenced by saturation of dietary fat
Rose McGovern, Forrest Ward Quackenbush
Abstract
Rose McGovern, Forrest Ward Quackenbush
Abstract
Abstract Injections of [24‐14C] chenodeoxycholate and3H‐cholate were made by heart puncture into 300 g male rats that bore T‐cannulas in their bile ducts. The animals had been raised on diet A, containing glucose, cholesterol and cholate, or diet B, containing sucrose and cholesterol; each of the diets contained 5% safflower oil or 5% beef tallow as variables. From analysis of bile samples collected from the T at intervals over a 5 day period, it was observed that the safflower oil group fed diet B had a 17% shorter cholate half‐life, a 29% larger cholate pool size and 52% higher rate of cholate synthesis than those fed beef tallow in the same diet. The safflower group fed diet A also had a larger cholate pool size, but synthesis and half‐life were obscured by cholate feeding. Chenodeoxycholate turnover data were not obtainable because the decay curves were bimodal for all treatments and hence did not conform to a simple pool model. It is concluded that dietary safflower oil causes more rapid formation of cholate than does dietary beef tallow in the cholesterol‐fed rat.
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Abstract Injections of [24‐14C] chenodeoxycholate and3H‐cholate were made by heart puncture into 300 g male rats that bore T‐cannulas in their bile ducts. The animals had been raised on diet A, containing glucose, cholesterol and cholate, or diet B, containing sucrose and cholesterol; each of the diets contained 5% safflower oil or 5% beef tallow as variables. From analysis of bile samples collected from the T at intervals over a 5 day period, it was observed that the safflower oil group fed diet B had a 17% shorter cholate half‐life, a 29% larger cholate pool size and 52% higher rate of cholate synthesis than those fed beef tallow in the same diet. The safflower group fed diet A also had a larger cholate pool size, but synthesis and half‐life were obscured by cholate feeding. Chenodeoxycholate turnover data were not obtainable because the decay curves were bimodal for all treatments and hence did not conform to a simple pool model. It is concluded that dietary safflower oil causes more rapid formation of cholate than does dietary beef tallow in the cholesterol‐fed rat.
Key concepts: Tallow, Cholesterol, Clinical chemistry, Lipidology, Safflower oil, Food science, Sodium Cholate, Biology