Abstract
Previous studies in humans have shown that the ingestion of lecithin can alter plasma cholesterol and triglyceride concentrations by mechanism(s) that remain to be elucidated. To further explore this response to lecithin, hyperlipemic rhesus monkeys were selected from a group of animals fed a semipurified diet containing corn oil, casein, sucrose and cholesterol (120 mg/100 Kcal) for 10 years. Soybean lecithin (92% phosphatidylcholine) was supplemented in the diet (0.5 g/100 Kcal) of these monkeys. Measurements of plasma cholesterol, triglycerides and phospholipid were made prior to, during and following 7 wk of lecithin supplementation. In addition, determinations of triglyceride secretion rates following administration of Triton WR1339, triglyceride clearance after intravenous infusion of Intralipid® and plasma lecithin:cholesterol acyl transferase enzyme (LCAT) activity were assessed at the same time intervals. As in other studies, manipulation of lecithin intake elicited a highly variable response, but significant changes were observed in plasma cholesterol and triglycerides as a consequence of supplementing or removing lecithin from the diet. Lecithin had no influence on the absolute plasma phospholipid level or LCAT activity. However, lecithin significantly reduced total lipids, increased the relative concentration of phospholipid and tended to increase the phospholipid/free cholesterol (PL/FC) concentration. While lecithin did not significantly affect triglyceride secretion rates, all animals were able to clear Intralipid® (triglyceride) more efficiently while fed lecithin. These data are interpreted to mean that the reduction in plasma lipids associated with lecithin ingestion may have been mediated via enhanced clearance of lipids transported in lipoproteins of lower density, whereas the rebound following lecithin removal reflected reduced clearance of these lipids.