title: Apolipoprotein E4 phenotype increases non-fasting serum triglyceride concentration in infants - the STRIP study.
abstract: As genetically determined apolipoprotein E (apo E) phenotypes influence serum cholesterol concentration, we analysed whether serum triglyceride values are also affected by the apo E phenotypes in infants. Non-fasting serum triglyceride values were measured in 7- and 13-month-old participants in the STRIP project, a randomised, prospective trial aimed at reducing children's exposure to known atherosclerosis risk factors (n=1062). The mean+/-S.D. non-fasting serum triglyceride concentrations in 7-month-old infants with apo E4/4 (n=36), E3/4 (n=209), E3/3 (n=412), and E2/3 (n=66) were 2. 05+/-1.24, 1.81+/-0.90, 1.63+/-0.90, and 1.71+/-0.83 mmol/l, respectively. Triglyceride concentrations were higher in infants with apo E4/4 or 3/4 than in those with apo E3/3 (P-value for difference 0.01 and 0.009, respectively). The apo E phenotype similarly influenced non-fasting serum triglyceride concentrations at the age of 13 months. The differences in serum triglyceride values in apo E4(+) infants (apo E3/4 and 4/4 infants combined) and apo E4(-) infants (apo E2/3 and 3/3 infants combined) occurred independently of the relative weight of the infant, milk type used at 7 months of age (breast milk or formula), and time elapsed from the previous meal. To conclude, apo E phenotypes regulate non-fasting serum triglyceride values in healthy infants. Apo E3/4 and apo E4/4 predispose infants to higher values than apo E3/3 phenotype, suggesting that the varepsilon4 allele may increase atherosclerosis risk also via it's effect on postprandial triglyceride metabolism.
authors.affiliation: Cardiorespiratory Research Unit, University of Turku, Kiinamyllynkatu 10, FIN-20520, Turku, Finland. anne.tammi@utu.fi
authors.forename: A
authors.initials: A
authors.lastname: Tammi
authors.forename: T
authors.initials: T
authors.lastname: Rönnemaa
authors.forename: J
authors.initials: J
authors.lastname: Viikari
authors.forename: E
authors.initials: E
authors.lastname: Jokinen
authors.forename: H
authors.initials: H
authors.lastname: Lapinleimu
authors.forename: C
authors.initials: C
authors.lastname: Ehnholm
authors.forename: O
authors.initials: O
authors.lastname: Simell
mesh_terms: D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000032:analysis* / Q000235:genetics*; D001161:Arteriosclerosis / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D001786:Blood Glucose / Q000032:analysis; D001942:Breast Feeding; D005215:Fasting / Q000097:blood; D005260:Female; D006801:Humans; D015994:Incidence; D007223:Infant; D008297:Male; D010641:Phenotype; D012016:Reference Values; D012307:Risk Factors; D012680:Sensitivity and Specificity; D014280:Triglycerides / Q000097:blood*
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D001786:Blood Glucose; D014280:Triglycerides