Arterial composition and metabolism: esterified fatty acids and cholesterol.

TLDR: In this article, the authors discuss the composition and metabolism of arteries to an understanding of the degeneration of esterified fatty acids and cholesterol and distinguish morphological changes in arteries with age and with atherosclerosis from changes that occur in the chemical composition of the arterial wall.

Abstract: Publisher Summary This chapter discusses the composition and metabolism of arteries to an understanding of the degeneration of esterified fatty acids and cholesterol. It is possible to distinguish the morphological changes that occur in arteries with age and with atherosclerosis from changes that occur in the chemical composition of the arterial wall. Some progress has been made in explaining changes in the chemical composition through biochemical mechanisms and through the prevalence of different subcellular components, each with its own characteristic composition. Hyperlipemia is not the only mechanism for inducing lesions that indiscriminately take up cholesterol esters from plasma, and hyperlipemia is not required to maintain a net uptake of cholesterol esters once advanced atherosclerotic lesions are established. Cholesterol esters perhaps accumulate in advanced lesions because they are the most prevalent nonpolar constituents of low density lipoproteins. The increase in lecithin concentrations in aortic tissue with experimental atherosclerosis is apparently not an early change and may be considered in association with the second stage in atherogenesis. The increase in lecithin concentrations may be secondary to increased lysolecithin concentrations and increased rates of lysolecithin acylation in the arterial tissue. The increased lysolecithin concentrations in aorta are in part the result of increased concentrations and rates of formation of lysolecithin in plasma. It seems likely that the most interesting and, perhaps, fruitful investigations of arterial lipids in the future will involve the early biochemical and ultrastructural changes prior to the development of the overt morphological changes of atherosclerosis.