Current understanding of placental fatty acid transport : Current Opinion in Clinical Nutrition & Metabolic Care (original) (raw)
PAEDIATRICS: Edited by Berthold V. Koletzko and Raanan Shamir
aService of Gynecology and Obstetrics, Virgen de la Arrixaca Hospital, Murcia, Spain
bDr von Haunersches Kinderspital, Ludwig-Maximilians University, Munich, Germany
cDepartment of Physiology, Faculty of Biology, University of Murcia, Murcia, Spain
Correspondence to Elvira Larqué, Department of Physiology, Faculty of Biology, University of Murcia, Campus Espinardo 30100, Murcia, Spain. Tel: +34 868884239; fax: +34 868883963; e-mail: [email protected]
Current Opinion in Clinical Nutrition and Metabolic Care 15(3):p 265-272, May 2012. | DOI: 10.1097/MCO.0b013e3283523b6e
Abstract
Purpose of review
The amount and activity of placental enzymes, receptors, and transport proteins will determine the extent of lipid transfer to the fetus that strongly contributes to fetal fat accretion.
Recent findings
Several studies have shown an association between the percentage of maternal plasma docosahexaenoic acid during gestation and the development of cognitive functions in the neonate. The functionality of the placenta could affect neonatal adiposity and fetal levels of long-chain polyunsaturated fatty acids in the offspring.
Summary
Both in-vitro and human in-vivo studies using labeled fatty acids (FAs) reported a preferential placental–fetal transfer of long-chain polyunsaturated fatty acids, although the mechanisms are still uncertain. The placenta uptakes the maternal circulating nonesterified fatty acids (NEFAs) and FAs released by maternal lipoprotein lipase and endothelial lipase. These NEFAs enter the cell through passive diffusion or by membrane carrier proteins. NEFAs bind to cytosolic fatty-acid-binding proteins to interact with subcellular organelles, including the endoplasmic reticulum, mitochondria, lipid droplets and peroxisomes. Knowledge about FA metabolism and adaptations in response to obesity or diabetes in human placenta is more limited, and contradictory results are available in their influence on placental lipases and carriers.
© 2012 Lippincott Williams & Wilkins, Inc.