Abstract
Intimamedia tissue from atherosclerotic rabbits showed a 15-fold increase in the amount of [U- 14C]palmitic acid oxidized to CO 2 compared to normal intimamedia. The findings suggest that oxidation of free fatty acids may at least in part contribute to the increased oxygen uptake seen in atherosclerotic tissue. The concentration of endogenous free fatty acids in atherosclerotic tissue was much higher than in normal tissue. The higher level may have been partly due to the increased levels of serum free fatty acid in the atherosclerotic rabbits, and to the increased permeability of atherosclerotic intimamedia to free fatty acids demonstrated in vitro. The tissue from atherosclerotic rabbit aortas exhibited a different pattern of fatty acid esterification than did that obtained from control aortas. In atherosclerotic tissue more cholesterol ester than triglyceride was formed from palmitate. In determining the specific activity of the free fatty acid tissue pool(s), equilibration of medium and tissue free fatty acid was found to be slow. In addition, the amount of free fatty acid in aorta was substantial and somewhat variable from animal to animal. Therefore, it was necessary to base calculations of fatty acid metabolic pathways on the specific activity of the palmitate in the tissue and not on that of the medium.
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