title: Dietary fat impacts fetal growth and metabolism: uptake of chylomicron remnant core lipids by the placenta.
abstract: The fetus requires significant energy for growth and development. Although glucose is a major source of energy for the fetus, other maternal nutrients also appear to promote growth. Thus, the goal of these studies was to determine whether triglyceride-rich remnants are taken up by the placenta and whether maternal dietary lipids, independently of adiposity, can impact fetal growth. To accomplish our first goal, chylomicron particles were duallly labeled with cholesteryl ester and triglycerides. The placenta took up remnant particles/core lipids at rates greater than adipose tissue and skeletal muscle but less than the liver. Although the placenta expresses apoE receptors, uptake of chylomicron remnants and/or core lipids can occur independently of apoE. To determine the impact of dietary lipid on fetal growth, independent of maternal adiposity, females were fed high-fat diets (HFD) for 1 mo; there was no change in adiposity or leptin levels prior to or during pregnancy of dams fed HFD. Fetal masses were greater in dams fed HFD, and mRNA levels of proteins involved in fatty acid oxidation (CPT I, PPARα), but not glucose oxidation (pyruvate kinase) or other regulatory processes (HNF-4α, LXR), were increased with maternal dietary fat. There was also no change in mRNA levels of proteins involved in placental glucose and fatty acid transport, and GLUT1 protein levels in microvillous membranes were similar in placentas of dams fed either diet. Thus, the ability of the placenta to take up chylomicron remnant core lipids likely contributes to accelerated fetal growth in females fed high fat diets.
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Cincinnati Medical School, 2180 E. Galbraith Rd., Cincinnati, OH 45237, USA.
authors.forename: Sandra L
authors.initials: SL
authors.lastname: Rebholz
authors.forename: Katie T
authors.initials: KT
authors.lastname: Burke
authors.forename: Qing
authors.initials: Q
authors.lastname: Yang
authors.forename: Patrick
authors.initials: P
authors.lastname: Tso
authors.forename: Laura A
authors.initials: LA
authors.lastname: Woollett
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics; D002250:Carbon Radioisotopes; D053298:Chylomicron Remnants / Q000493:pharmacokinetics*; D004041:Dietary Fats / Q000493:pharmacokinetics*; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D060752:Fetuin-B; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000378:metabolism; D014316:Tritium; D000509:alpha-Fetoproteins / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D002250:Carbon Radioisotopes; D053298:Chylomicron Remnants; D004041:Dietary Fats; C504687:FETUB protein, human; D060752:Fetuin-B; D014280:Triglycerides; D000509:alpha-Fetoproteins; D014316:Tritium