title: Postprandial triglyceride response in young adult men and familial risk for coronary atherosclerosis.
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.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  Coronary angiography departments of four central general hospitals in the Netherlands.
  
  
  METHODS
  80 sons (mean age, 24.8 years) of men with severe coronary artery disease and 55 sons (mean age, 23.2 years) of controls.
  
  
  METHODS
  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.
authors.affiliation: Erasmus University Medical School, Rotterdam, The Netherlands.
authors.forename: C S
authors.initials: CS
authors.lastname: Uiterwaal
authors.forename: D E
authors.initials: DE
authors.lastname: Grobbee
authors.forename: J C
authors.initials: JC
authors.lastname: Witteman
authors.forename: W A
authors.initials: WA
authors.lastname: van Stiphout
authors.forename: X H
authors.initials: XH
authors.lastname: Krauss
authors.forename: L M
authors.initials: LM
authors.lastname: Havekes
authors.forename: A M
authors.initials: AM
authors.lastname: de Bruijn
authors.forename: A
authors.initials: A
authors.lastname: van Tol
authors.forename: A
authors.initials: A
authors.lastname: Hofman
mesh_terms: D000328:Adult; D003324:Coronary Artery Disease / Q000097:blood* / Q000235:genetics*; D003430:Cross-Sectional Studies; D004041:Dietary Fats / Q000008:administration & dosage; D004224:Diterpenes; D004435:Eating; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D009679:Nuclear Family; D000084562:Retinyl Esters; D012307:Risk Factors; D013997:Time Factors; D014280:Triglycerides / Q000097:blood*; D014801:Vitamin A / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D004041:Dietary Fats; D004224:Diterpenes; D008055:Lipids; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate