Die invloed van 'n verhoogde eierinname op die in vitro-sintese van tromboksaan en verwante metaboliete

Abstract

Coronary heart disease (CHD ) is a multi-factorial disease in which many risk factors can enhance the genetic potential to develop the disease (Vorster et al.,198&9). These risk factors are especially associated with a Western lifestyle. In the past, the approach to diet as a risk factor largely focused on a lowering of dietary fats and cholesterol. The extent to which increased intakes of dietary cholesterol contribute to an increase in serumcholesterol levels, is still controversial. Recent epidemiological, clinical and experimental studies have indicated that an enhanced coagulant activity (raised levels of plasma fibrinogen and factor VII) also increases the risk of atherosclerosis and CHD (Meade et al., 1986). An aspect which has not received attention in the literature is the possible effect of an enhanced egg intake on the eicosanoid metabolism. The primary precursor of the eicosanoids is arachidonic acid, a poli-unsaturated fatty acid which is absorbed in the diet or which is synthesized in the body from diet linoleic acid (Hecker & Ullrich,1989) The eicosanoids may be involved in the development of CHD. The main objective of this study was to examine the effect of an increased egg ( and therefore arachidonic acid) intake on aspects of eicosanoid metabolism in 30 healthy young male students. After a run-in period of 2 months during which all the subjects ate 3 eggs per week, the subjects were divided into three groups. Group 1 (reference group) continued eating three eggs per week, group 2 ate 7 eggs per week and group 3, 14 eggs per week for one month. Measurements were made at baseline and after one month. The ability of blood platelets to synthesize eicosanoids (TXB:a, HHT and 12-HETE) from arachidonic acid on a low and high egg intake was examined. Additionally, the influence of an enhanced egg intake on serumlipids and lipoproteins, haemostatic variables, as well as various other variables were also investigated.

The results of this study indicated that there were no significant changes in arachidonic acid in the plasmatriglycerides. The experimental groups all showed an increase in the eicosanoid index ( 3 H-arachidonic acid converted to 3 H-thromboxane\ 3 H-HHT\ 3 H-12-HETE per platelet count), possibly a joint result of normal variations and experimental circumstances. The enhanced egg intake did not have an effect on the lipid profile of the experimental subjects, possibly because of the activity of the enzyme lecithin-cholesterol-acetyl-transferase. No significant changes in the coagulant activity were noted . It seems therefore that the intake of 3-14 eggs per week did not influence the risk factors of CHD in these healthy, young male subjects.