title: Maternal and fetal cord blood lipids in intrauterine growth restriction.
abstract: OBJECTIVE
  Small for gestational age neonates (SGA) could be subdivided into two groups according to the underlying causes leading to low birth weight. Intrauterine growth restriction (IUGR) is a pathologic condition with diminished growth velocity and fetal compromised well-being, while non-growth restricted SGA neonates are constitutionally (genetically determined) small. Antenatal sonographic measurements are used to differentiate these two subgroups. Maternal metabolic changes contribute to the pathogenesis of IUGR. A disturbed lipid metabolism and cholesterol supply might affect the fetus, with consequences for fetal programming of cardiovascular diseases. We evaluated fetal serum lipids and hypothesized a more atherogenic lipoprotein profile in IUGR fetuses.
  
  
  METHODS
  Umbilical cord serum lipids and oxidative modified, low-density lipoprotein (oxLDL) concentrations were measured by colorimetric enzymatic measurements, or by ELISA. Values of IUGR (n=36) and constitutionally small for gestational age neonates (SGA, n=22) were compared with those of healthy, adequate for gestational age, born neonates (CN, n=97). SAS-statistic software was used and two-way ANOVA was adjusted for gestational age at delivery.
  
  
  RESULTS
  Fetal high-density lipoprotein cholesterol (HDL-C) and total cholesterol (TC) concentrations were found to be lower in the IUGR compared to the CN and SGA groups (HDL-C: P<0.001, TC: P<0.01). Atherogenic indices, including the oxLDL/LDL-C ratio, were increased in the IUGR compared to the CN group (oxLDL/LDL-C ratio: P<0.001).
  
  
  CONCLUSIONS
  Our results support the hypothesis of a disturbed cholesterol supply in IUGR fetuses. Born SGA has been shown to be a risk factor for developing cardiovascular disease later in life. Since HDL-C has anti-inflammatory properties, a reduced HDL-C during fetal development, and an increase in atherogenic indices, might provide a link to this observation in IUGR fetuses.
authors.affiliation: Department of Obstetrics and Gynecology of the University Hospital of the RWTH Aachen, Germany. upecks@ukaachen.de
authors.forename: Ulrich
authors.initials: U
authors.lastname: Pecks
authors.forename: Meike
authors.initials: M
authors.lastname: Brieger
authors.forename: Barbara
authors.initials: B
authors.lastname: Schiessl
authors.forename: Dirk O
authors.initials: DO
authors.lastname: Bauerschlag
authors.forename: Daniela
authors.initials: D
authors.lastname: Piroth
authors.forename: Benjamin
authors.initials: B
authors.lastname: Bruno
authors.forename: Christina
authors.initials: C
authors.lastname: Fitzner
authors.forename: Thorsten
authors.initials: T
authors.lastname: Orlikowsky
authors.forename: Nicolai
authors.initials: N
authors.lastname: Maass
authors.forename: Werner
authors.initials: W
authors.lastname: Rath
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005317:Fetal Growth Retardation / Q000097:blood*; D006801:Humans; D007231:Infant, Newborn / Q000097:blood; D007236:Infant, Small for Gestational Age / Q000097:blood; D008055:Lipids / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D011225:Pre-Eclampsia / Q000097:blood; D011247:Pregnancy / Q000097:blood; D012016:Reference Values; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D008077:Lipoproteins, LDL; D014280:Triglycerides; C099252:oxidized low density lipoprotein; D002784:Cholesterol