Dietary Lecithin: Metabolism, Fate, and Effects on Metabolism of Lipids and Lipoproteins

Abstract

The phospholipids, of which lecithin is a major component, constitute a major class of lipids in body tissues and in plasma. They play a vital role in cellular function and in transport of lipids. Since they are required for the solubilization of cholesterol, both within cells and in lipoproteins, the question naturally has arisen whether the phospholipids, or lecithin in particular, can be used in the prevention of atherosclerosis. This possibility has led investigators to feed phospholipids and to administer them intravenously with the aim of slowing down the process of atherosclerosis. Results have been conflicting. Some studies in experimental animals have suggested that the feeding of lecithin can reduce the size of atherosclerotic plaques (1,2). Several mechanisms might be responsible for this effect. There could be an increase in the activities of cholesteryl ester hydrolase in the arterial wall (3,4); there might be an activation of triglyceride lipase (5); or there could be changes in the metabolism of high density lipoproteins (HDL) (6). Further, high doses of lecithin in the diet might interfere with absorption of cholesterol, or they might alter the metabolism of triglycerides or low density lipoproteins (LDL). Because of the possible beneficial effects of dietary lecithin, our laboratory has carried out a series of studies on the metabolism of lecithin. Although these studies have not specifically examined whether the feeding of lecithin will prevent the development of atherosclerosis, they have provided new insights into the metabolism of lecithin and the effects of lecithin on the metabolism of other lipids. Our findings will be summarized in this chapter.