The purpose of the present study was to assess the role of the liver in the plasma-cholesterol-lowering effect of soyabean lecithin. Normolipidaemic rats were fed on lecithin-enriched or control diets with the same amount of protein. The lecithin diets contained 200 g/kg high-fat commercial semi-purified soyabean lecithin (230 g/kg total lipids as soyabean phosphatidylcholine) or 200 g/kg high-fat purified soyabean lecithin (930 g/kg total lipids as soyabean phosphatidylcholine). The control diets were a lowfat diet (40 g fat/kg) and a high-fat triacylglycerol-rich diet (200 g fat/kg). The high-fat diets were isoenergetic. The cholesterol-lowering effect of the lecithin-enriched diets was associated with significantly lower levels of plasma total-and HDL-cholesterol and significantly higher levels of bile phosphatidylcholine (PC), bile salts and cholesterol. These findings suggest that the liver plays a major role in the reduction of plasma cholesterol, the increased biliary lipid being provided by both HDL and the hepatic microsomal pools of PC and cholesterol.
Many studies in humans volunteers have shown that dietary docosahexaenoic acid (DHA) supplied as triacylglycerol can increase DHA levels in blood lipids but often strongly decreases those of arachidonic acid (AA). The aim of the present study was to determine the effect of dietary supplementation with egg-yolk powder enriched in DHA, corresponding to the French recommended dietary allowance for DHA, on the blood lipid status of an elderly population. Institutionalised elderly individuals aged between 63 and 93 years consumed an egg product enriched in DHA (150 mg/d) once daily for 9 months. Plasma lipids and the fatty acid composition of erythrocyte membranes were determined every 3 months. The supplementation induced an increase in the PUFA content of plasma and erythrocyte membranes which was þ 14·5 and þ25·3 %, respectively, at 9 months. This effect was mainly due to the level of DHA and, unexpectedly, to that of AA which continuously increased. This increase in AA was the result of an increased dietary intake (þ50 mg/d) and very probably of an increased biosynthesis as demonstrated by the behaviour of di-homo-g-linolenic acid. The supplementation resulted in a blood PUFA status comparable with that of young healthy controls. The data are consistent with a strong regulatory action of the dietary treatment on the subjects' lipid metabolism.
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