Currently atherosclerosis is the number - one cause of death worldwide including Thailand. Hyperlipidaemia is an important etiology of atheroma formation and thrombosis leading to atherosclerotic occlusion. Platelet aggregation plays an important role to contribute to microthrombus formation. The type of fats is closely related to atherosclerosis and thrombosis. There is some evidence suggesting that medium chain triglycerides ( MCT ) may alter platelet function in opposite direction to that altered by long - chain triglyceride ( LCT ) in some favorable way since MCT does not produce post - prandial lipaemia and is not precursor of prostaglandins. This speculation has never been tested. The purpose of this study was designed to investigate the acute effect of MCT on platelet buoyancy, aggregation and morphology. The ultimate aim is to investigate whether MCT is beneficial with regard to prevention of atherosclerosis. Fourteen healthy young men were the subjects of the study. They were randomly assigned to consume 65g. LCT or equicaloric amount of MCT incorporated into an artificial milk and margarine spread over four slices of bread. The assignment was made in a cross-over fashion. If a subject was begun on one of the two fats, he would automatically be given the other fat one week later. Blood was drawn at 0, 31/2 and 7 hours for determination of serum triglycerides, cholesterol, acetoacetic acid, - hydroxybutyric acid, platelet buoyancy following ultracentrifugation , platelet aggregation in response to different concentr ation s of ADP, adrenaline and collagen and platelet morphology under scanning and transmission electron microscopes. The results are as follow: (1) LCT induced elevation of serum triglycerides in contrast to MCT which did not. (2) Both MCT and LCT induced hyperketonemia but the former induced it to a much greater degree particularly at 31/2 hours than the latter. (3) Upon ultracentrifugation LCT increased platelet number in the top layer plasma. This finding is probably secondary to increased viscosity of plasma and floatation of chylomicron, and is indicative of increased platelet buoyancy. MCT did not increase platelet number in the top layer plasma implying that platelets were not buoyant. (4) Platelet aggregation was determined in PRP both with and without standardization of number of platelets to 250,000 cell/ul With adjusted PRP ingestion of LCT or MCT did not induce any changes in various parameters of platelet aggregation in response to different aggregating agents at differing concentrations. With unadjusted PRP ingestion of LCT significantly decreased platelet aggregation in response to 6uM ADP, and to collagen at 0.08 and 0.16mg/ml PRP while ingestion of MCT significantly increased platelet aggregation in response to collagen at 0.08 mg/ml PRP. The apparent favorable effect of LCT in decreasing platelet aggregation may be an artifact resulting from postprandial turbidity following ingestion of LCT. Further study with whole blood impedance method rather than plasma optical method will provide a more definite answer regarding which fat LCT or MCT has a beneficial effect on platelet aggregation. (5) Both MCT and LCT did not affect any discenable change in the platelet morphology by SEM. (6) Engulfment of fat droplets as evident in TEM after LCT ingestion was increased while that after MCT ingestion did not.