title: The role of angiotensin-converting enzyme and apolipoprotein-E gene polymorphisms on lipid compositions in newborn infants with intrauterine growth restriction.
abstract: Recent findings suggest that hypertension, dyslipidemia, diabetes mellitus, coronary heart disease are more common in adults who born with intrauterine growth restriction (IUGR). Several studies have shown that polymorphisms in angiotensin-converting enzyme (ACE) and apolipoprotein-E (Apo-E) are effective in developing the insulin resistance and also in increasing the risk of coronary heart disease. In present study, the frequencies of ACE, Apo-E gene polymorphisms, apolipoprotein-B (Apo-B) mutation and lipid compositions were determined in full-term newborn infants with IUGR. Forty-four newborn infants who had completed 36 weeks of gestational age, 24 healthy infants and 20 with IUGR, were taken into the scope of the study. While total cholesterol (TC) and Apo-B concentrations in infants with IUGR was found to be significantly higher than that of the control group (p<0.05), triglyceride (TG), low-density lipoproteins (LDL), high-density lipoproteins (HDL) and Apo-A1 levels were similar (p>0.05). An insertion/deletion (I/D) polymorphism with a significantly increased frequency was observed in the IUGR group (65%) as compared with the control group (33%) (p<0.05). When the distribution of the Apo-E gene polymorphism (E2, E3 and E4) was studied, no difference was found between the IUGR and control groups with respect to frequency. No Apo-B gene mutation was identified in the study groups. In conclusion, we may suggest that I/D polymorphism is responsible, though in part, for the etiology of intrauterine growth restriction. Levels of total cholesterol and Apo-B are elevated in IUGR infants, suggesting a linkage between low birth weight and atherosclerosis.
authors.affiliation: Department of Pediatrics, Ege University Medical School, Bornova, Izmir 35100, Turkey. makisu@med.ege.edu.tr
authors.forename: Mete
authors.initials: M
authors.lastname: Akisu
authors.forename: Zuhal
authors.initials: Z
authors.lastname: Balim
authors.forename: Hasan
authors.initials: H
authors.lastname: Cetin
authors.forename: Buket
authors.initials: B
authors.lastname: Kosova
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yalaz
authors.forename: Nejat
authors.initials: N
authors.lastname: Topcuoglu
authors.forename: Nilgun
authors.initials: N
authors.lastname: Kultursay
mesh_terms: D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism; D004252:DNA Mutational Analysis; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics* / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D008074:Lipoproteins / Q000145:classification / Q000235:genetics* / Q000378:metabolism; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic
chemical_list: D001057:Apolipoproteins E; D008074:Lipoproteins; D007703:Peptidyl-Dipeptidase A