title: Abnormal postprandial apolipoprotein B-48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study.
abstract: Because remnants of triglyceride-rich lipoproteins (TRLP) are potentially atherogenic, the postprandial lipoprotein metabolism was studied in 12 normocholesterolemic, normotriglyceridemic women, aged 60 +/- 2 years, with angiographically proven coronary artery disease (CAD+; cholesterol 5.7 +/- 0.1 (S.E.) mmol/l, triglyceride 1.35 +/- 0.10 mmol/l) and in 12 individually matched controls, aged 59 +/- 2 years, without angiographical abnormalities (CAD-; cholesterol 5.1 +/- 0.2 mmol/l and triglyceride 1.16 +/- 0.13 mmol/l). Following an oral retinyl palmitate-fat load, the CAD+ women showed a significantly higher triglyceride response in the chylomicron, or Sf > 1000, fraction (P < 0.05 vs. controls). Total plasma apolipoprotein (apo) B and retinyl palmitate concentrations were similar in both groups. Fasting apo B-48 levels in the d < 1.006 g/ml fraction were significantly higher in CAD+ cases (0.25 +/- 0.03 integrated optical density (iod) units) than CAD- controls (0.15 +/- 0.03; P < 0.05). Furthermore, after the fat load, a greater absolute and incremental apo B-48 response in the intermediate density lipoprotein (IDL) fraction (d = 1.006-1.019 g/ml) was observed in CAD+ cases (incremental area under the curve (Delta-AUC)8: 0.40 +/- 0.12 h.iod) than CAD- controls (0.01 +/- 0.06 h.iod; P = 0.01). Post-heparin hepatic lipase (HL) activities were higher in the CAD+ group: 422 +/- 22 mU/l vs 288 +/- 20 mU/ml in the CAD- group (P < 0.001) while lipoprotein lipase (LPL) activities were identical. The results provide evidence that the metabolism of intestinal TRLP is significantly different in normolipidemic women with angiographically proven CAD compared with individually matched controls without coronary disease. Fasting apo B-48 levels in d< 1.006 g/ml fractions represent a potentially useful marker in women at risk for CAD.
authors.affiliation: Department of Internal Medicine and Endocrinology, Academic Hospital, Utrecht, The Netherlands.
authors.forename: E
authors.initials: E
authors.lastname: Meyer
authors.forename: H T
authors.initials: HT
authors.lastname: Westerveld
authors.forename: F C
authors.initials: FC
authors.lastname: de Ruyter-Meijstek
authors.forename: M M
authors.initials: MM
authors.lastname: van Greevenbroek
authors.forename: R
authors.initials: R
authors.lastname: Rienks
authors.forename: H J
authors.initials: HJ
authors.lastname: van Rijn
authors.forename: D W
authors.initials: DW
authors.lastname: Erkelens
authors.forename: T W
authors.initials: TW
authors.lastname: de Bruin
mesh_terms: D000704:Analysis of Variance; D000925:Anticoagulants / Q000627:therapeutic use; D053283:Apolipoprotein B-48; D001055:Apolipoproteins B / Q000097:blood*; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy; D004224:Diterpenes; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood; D053419:Lipoproteins, IDL; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D019518:Postprandial Period / Q000502:physiology*; D011863:Radioimmunoassay; D000084562:Retinyl Esters; D012189:Retrospective Studies; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*; D014461:Ultracentrifugation; D014801:Vitamin A / Q000031:analogs & derivatives* / Q000097:blood
chemical_list: D000925:Anticoagulants; D053283:Apolipoprotein B-48; D001055:Apolipoproteins B; D004224:Diterpenes; D008074:Lipoproteins; D053419:Lipoproteins, IDL; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate; D006493:Heparin; D002784:Cholesterol; D008071:Lipoprotein Lipase