title: Placental adaptations in growth restriction.
abstract: The placenta is the primary interface between the fetus and mother and plays an important role in maintaining fetal development and growth by facilitating the transfer of substrates and participating in modulating the maternal immune response to prevent immunological rejection of the conceptus. The major substrates required for fetal growth include oxygen, glucose, amino acids and fatty acids, and their transport processes depend on morphological characteristics of the placenta, such as placental size, morphology, blood flow and vascularity. Other factors including insulin-like growth factors, apoptosis, autophagy and glucocorticoid exposure also affect placental growth and substrate transport capacity. Intrauterine growth restriction (IUGR) is often a consequence of insufficiency, and is associated with a high incidence of perinatal morbidity and mortality, as well as increased risk of cardiovascular and metabolic diseases in later life. Several different experimental methods have been used to induce placental insufficiency and IUGR in animal models and a range of factors that regulate placental growth and substrate transport capacity have been demonstrated. While no model system completely recapitulates human IUGR, these animal models allow us to carefully dissect cellular and molecular mechanisms to improve our understanding and facilitate development of therapeutic interventions.
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. song.zhang@unisa.edu.au.
authors.forename: Song
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Departments of Obstetrics and Gynecology, University of Western Ontario, London, ON N6A 5C1, Canada. tim.regnault@uwo.ca.
authors.forename: Timothy R H
authors.initials: TR
authors.lastname: Regnault
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. barpl002@mymail.unisa.edu.au.
authors.forename: Paige L
authors.initials: PL
authors.lastname: Barker
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. kb555@cam.ac.uk.
authors.forename: Kimberley J
authors.initials: KJ
authors.lastname: Botting
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. caroline.mcMillen@newcastle.edu.au.
authors.forename: Isabella C
authors.initials: IC
authors.lastname: McMillen
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. mcmcm003@mymail.unisa.edu.au.
authors.forename: Christine M
authors.initials: CM
authors.lastname: McMillan
authors.affiliation: The Robinson Research Institute, University of Adelaide, Adelaide, SA 5005, Australia. claire.roberts@adelaide.edu.au.
authors.forename: Claire T
authors.initials: CT
authors.lastname: Roberts
authors.affiliation: Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. janna.morrison@unisa.edu.au.
authors.forename: Janna L
authors.initials: JL
authors.lastname: Morrison
mesh_terms: D000222:Adaptation, Physiological; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation; D005947:Glucose / Q000378:metabolism; D006801:Humans; D023421:Models, Animal; D008954:Models, Biological; D010920:Placenta / Q000503:physiopathology*; D011247:Pregnancy
chemical_list: D000596:Amino Acids; D005227:Fatty Acids; D005947:Glucose