title: Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.
abstract: A delayed clearance of postprandial lipoproteins from the plasma may play a role in the etiology of premature coronary atherosclerosis. To address this hypothesis, we studied chylomicron (remnant) metabolism in two groups of 20 selected normolipidemic men aged 35-65 years, a group of coronary artery disease (CAD) patients, and a matched control group with documented minimal coronary atherosclerosis. Subjects received an oral fat load supplemented with cholesterol and retinyl palmitate. Plasma samples obtained during the next 24-hour period were analyzed for total as well as d less than 1.019 g/ml and d greater than 1.019 g/ml triacylglycerol, cholesterol, and retinyl ester concentrations. Although both groups of patients responded identically in terms of the appearance of gut-derived lipids in the plasma, CAD patients showed a marked delay in the clearance of retinyl esters as well as in the normalization of plasma triacylglycerol concentrations. Postheparin plasma hepatic lipase activity was significantly lower in the CAD group. Apolipoprotein E phenotype measurements did not reveal marked differences in frequency between both groups. The frequency distribution was not unusual in comparison with the normal Dutch population. The magnitude of the postprandial responses of triacylglycerol and retinyl esters was correlated positively with the fasting levels of plasma triacylglycerol and negatively with high density lipoprotein subfraction 2 cholesterol concentrations. These data indicate that the clearance of postprandial lipoproteins in normolipidemic CAD patients as selected in the present study is delayed as compared with that of controls without coronary atherosclerosis and suggest that postprandial lipoproteins may play a role in the etiology of their disease.
authors.affiliation: Department of Biochemistry, Erasmus University Rotterdam, The Netherlands.
authors.forename: P H
authors.initials: PH
authors.lastname: Groot
authors.forename: W A
authors.initials: WA
authors.lastname: van Stiphout
authors.forename: X H
authors.initials: XH
authors.lastname: Krauss
authors.forename: H
authors.initials: H
authors.lastname: Jansen
authors.forename: A
authors.initials: A
authors.lastname: van Tol
authors.forename: E
authors.initials: E
authors.lastname: van Ramshorst
authors.forename: S
authors.initials: S
authors.lastname: Chin-On
authors.forename: A
authors.initials: A
authors.lastname: Hofman
authors.forename: S R
authors.initials: SR
authors.lastname: Cresswell
authors.forename: L
authors.initials: L
authors.lastname: Havekes
mesh_terms: D000328:Adult; D001057:Apolipoproteins E / Q000097:blood; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood; D002914:Chylomicrons / Q000097:blood; D003327:Coronary Disease / Q000097:blood*; D004041:Dietary Fats / Q000008:administration & dosage; D004224:Diterpenes; D005502:Food; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D008049:Lipase / Q000097:blood; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D053439:Lipoproteins, HDL2; D008297:Male; D008875:Middle Aged; D000084562:Retinyl Esters; D014280:Triglycerides / Q000097:blood; D014801:Vitamin A / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D002914:Chylomicrons; D004041:Dietary Fats; D004224:Diterpenes; D008055:Lipids; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D053439:Lipoproteins, HDL2; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate; D006493:Heparin; D002784:Cholesterol; D008049:Lipase