Postprandial Triglyceride Response in Young Adult Men and Familial Risk for Coronary Atherosclerosis

  1. Cuno S. P. M. Uiterwaal, MD;
  2. Diederick E. Grobbee, MD, PhD;
  3. Jacqueline C. M. Witteman, PhD;
  4. Willy-Anne H. J. van Stiphout, MD, PhD;
  5. Xeno H. Krauss, MD, PhD;
  6. Louis M. Havekes, PhD;
  7. Anthony M. de Bruijn, MSc;
  8. Arie van Tol, PhD; and
  9. Albert Hofman, MD, PhD
  1. Erasmus University Medical School, Rotterdam. Zuiderziekenhuis, Rotterdam. TNO Institute for Aging and Vascular Research, Gaubius Laboratory, Leiden, the Netherlands. Requests for Reprints: C.S.P.M. Uiterwaal, MD, Erasmus University Medical School, Department of Epidemiology & Biostatistics, P.O. Box 1738, 3000 DR Rotterdam, the Netherlands. Acknowledgments: The authors thank Ms. Lorette O.M. Hulsman for assistance with conducting the study, Ms. Jeannette M. Vergeer-Drop for assistance in laboratory analyses, and cardiologists Dr. H.J. Kingma (Antonius Ziekenhuis, Nieuwegein, the Netherlands), Dr. Ph.W. Fels (Refaja Ziekenhuis, Dordrecht, the Netherlands), and Dr. F.J. ten Cate (University Hospital, Rotterdam, the Netherlands) for helping select the patients. Grant Support: By grant 87058 from the Netherlands Heart Foundation.

    Abstract

    Objective: To determine whether an increased familial risk for coronary artery disease in young adult men is related to changes in postprandial lipoprotein metabolism.

    Design: Cross-sectional study.

    Setting: Coronary angiography departments of four central general hospitals in the Netherlands.

    Patients: 80 sons (mean age, 24.8 years) of men with severe coronary artery disease and 55 sons (mean age, 23.2 years) of controls.

    Measurements: Postprandial levels of serum triglycerides, retinyl palmitate, and total cholesterol were measured during a 12-hour period after a standardized oral lipid load.

    Results: Both groups showed a marked increase in levels of serum triglyceride and retinyl palmitate after lipid loading, reaching a maximum 4 to 6 hours postprandially. No changes in postprandial total cholesterol levels were observed in either group. Sons of men with coronary artery disease had prolonged postprandial hypertriglyceridemia when compared with sons of controls. Significant differences in postprandial triglyceride levels were found at 8 hours (difference, 0.35 mmol/L; 95% CI, 0.07 to 0.62 mmol/L), at 10 hours (difference, 0.21 mmol/L; CI, 0.06 to 0.36 mmol/L), and at 12 hours after lipid loading (difference, 0.13 mmol/L; CI, 0.01 to 0.26 mmol/L). Levels of postprandial retinyl palmitate were also slightly, but not statistically, different (mainly after 6 hours).

    Conclusions: Healthy young adult sons, whose fathers have established coronary artery disease, have prolonged postprandial hypertriglyceridemia. Changes in postprandial lipoprotein metabolism appear to be associated with familial risk for coronary atherosclerosis.

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