title: Postprandial response to a fat tolerance test in young adults with a paternal history of premature coronary heart disease - the EARS II study (European Atherosclerosis Research Study).
abstract: BACKGROUND
  The European Atherosclerosis Research Study (EARS) I had shown that fasting plasma concentrations of apolipoprotein B (apo B) and triglycerides were the most discriminant variables between offspring with a paternal history of coronary heart disease (CHD) and controls. The EARS II study was undertaken to investigate whether a paternal history of CHD was associated with differences in postprandial lipemia.
  
  
  METHODS
  Male subjects with a paternal history of CHD (cases, n = 407) and age-matched male controls (n = 415) were recruited from 14 European universities. All subjects had an oral fat tolerance test.
  
  
  RESULTS
  In the sample as a whole, the postprandial triglyceride responses did not significantly differ between the two groups. However, in the upper tertile of fasting triglycerides, cases displayed a higher area under the curve (5.71 vs. 4.49 mmol.h L-1, P < 0.001), a higher peak (1.76 vs. 1.43 mmol L-1, P < 0.001) and a more delayed time to peak (3.15 vs. 2.91 h, P < 0.05) than controls. In the upper tertile, fasting apo B levels (P < 0.05) and triglyceride area under the curve (P = 0.002) significantly discriminated cases from controls in a multivariate analysis. Cases had also higher Lp C-III:B levels at 4 h than controls (11.2 vs. 9.9 mg dL-1, P < 0.01) and this difference remained significant after adjustment for apo B and triglyceride levels.
  
  
  CONCLUSIONS
  These results indicate that in subjects with a moderate elevation of fasting triglycerides, an impaired postprandial response to a fat load constitutes an early biological expression of a paternal history of premature CHD.
authors.affiliation: INSERM U525, Paris, France. tiret@idf.inserm.fr
authors.forename: L
authors.initials: L
authors.lastname: Tiret
authors.forename: C
authors.initials: C
authors.lastname: Gerdes
authors.forename: M J
authors.initials: MJ
authors.lastname: Murphy
authors.forename: J
authors.initials: J
authors.lastname: Dallongeville
authors.forename: V
authors.initials: V
authors.lastname: Nicaud
authors.forename: D S
authors.initials: DS
authors.lastname: O'Reilly
authors.forename: U
authors.initials: U
authors.lastname: Beisiegel
authors.forename: G
authors.initials: G
authors.lastname: De Backer
mesh_terms: D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D053305:Apolipoprotein C-III; D001055:Apolipoproteins B / Q000097:blood; D001056:Apolipoproteins C / Q000097:blood; D001057:Apolipoproteins E / Q000097:blood; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000235:genetics; D003327:Coronary Disease / Q000175:diagnosis* / Q000235:genetics*; D004041:Dietary Fats / Q000008:administration & dosage / Q000097:blood; D005192:Family Health; D005220:Fathers; D020022:Genetic Predisposition to Disease; D006801:Humans; D016015:Logistic Models; D008297:Male; D019518:Postprandial Period; D011237:Predictive Value of Tests; D014280:Triglycerides / Q000097:blood
chemical_list: D053305:Apolipoprotein C-III; D001055:Apolipoproteins B; D001056:Apolipoproteins C; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004041:Dietary Fats; D014280:Triglycerides