The neglected role of insulin‐like growth factors in the maternal circulation regulating fetal growth

Maternal insulin‐like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating IGFs influence maternal tissue growth and metabolism, thereby regulating nutrient availability for the growth of the conceptus. Maternal IGFs...

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Published in:The Journal of physiology Vol. 589; no. 1; pp. 7 - 20
Main Authors: Sferruzzi‐Perri, A. N., Owens, J. A., Pringle, K. G., Roberts, C. T.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01.01.2011
Wiley Subscription Services, Inc
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ISSN:0022-3751, 1469-7793, 1469-7793
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Abstract Maternal insulin‐like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating IGFs influence maternal tissue growth and metabolism, thereby regulating nutrient availability for the growth of the conceptus. Maternal IGFs also regulate placental morphogenesis, substrate transport and hormone secretion, all of which influence fetal growth either via indirect effects on maternal substrate availability, or through direct effects on the placenta and its capacity to supply nutrients to the fetus. The extent to which IGFs influence the mother and/or placenta are dependent on the species and maternal factors, including age and nutrition. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing degenerative diseases in adult life, understanding the role of maternal IGFs during pregnancy is essential in order to identify mechanisms underlying altered fetal growth and offspring programming.
AbstractList Maternal insulin-like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating IGFs influence maternal tissue growth and metabolism, thereby regulating nutrient availability for the growth of the conceptus. Maternal IGFs also regulate placental morphogenesis, substrate transport and hormone secretion, all of which influence fetal growth either via indirect effects on maternal substrate availability, or through direct effects on the placenta and its capacity to supply nutrients to the fetus. The extent to which IGFs influence the mother and/or placenta are dependent on the species and maternal factors, including age and nutrition. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing degenerative diseases in adult life, understanding the role of maternal IGFs during pregnancy is essential in order to identify mechanisms underlying altered fetal growth and offspring programming.
Maternal insulin-like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating IGFs influence maternal tissue growth and metabolism, thereby regulating nutrient availability for the growth of the conceptus. Maternal IGFs also regulate placental morphogenesis, substrate transport and hormone secretion, all of which influence fetal growth either via indirect effects on maternal substrate availability, or through direct effects on the placenta and its capacity to supply nutrients to the fetus. The extent to which IGFs influence the mother and/or placenta are dependent on the species and maternal factors, including age and nutrition. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing degenerative diseases in adult life, understanding the role of maternal IGFs during pregnancy is essential in order to identify mechanisms underlying altered fetal growth and offspring programming.Maternal insulin-like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating IGFs influence maternal tissue growth and metabolism, thereby regulating nutrient availability for the growth of the conceptus. Maternal IGFs also regulate placental morphogenesis, substrate transport and hormone secretion, all of which influence fetal growth either via indirect effects on maternal substrate availability, or through direct effects on the placenta and its capacity to supply nutrients to the fetus. The extent to which IGFs influence the mother and/or placenta are dependent on the species and maternal factors, including age and nutrition. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing degenerative diseases in adult life, understanding the role of maternal IGFs during pregnancy is essential in order to identify mechanisms underlying altered fetal growth and offspring programming.
Author Pringle, K. G.
Owens, J. A.
Roberts, C. T.
Sferruzzi‐Perri, A. N.
Author_xml – sequence: 1
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  surname: Owens
  fullname: Owens, J. A.
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  givenname: K. G.
  surname: Pringle
  fullname: Pringle, K. G.
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  givenname: C. T.
  surname: Roberts
  fullname: Roberts, C. T.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20921199$$D View this record in MEDLINE/PubMed
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Snippet Maternal insulin‐like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating...
Maternal insulin-like growth factors (IGFs) play a pivotal role in modulating fetal growth via their actions on both the mother and the placenta. Circulating...
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StartPage 7
SubjectTerms Animals
Birth weight
Energy Metabolism
Female
Fetal Development
Fetus - blood supply
Fetus - metabolism
Health risk assessment
Humans
Insulin-like growth factors
Maternal Nutritional Physiological Phenomena
Maternal-Fetal Exchange
Placenta
Placenta - blood supply
Placenta - metabolism
Placental Circulation
Pregnancy
Prenatal development
Somatomedins - metabolism
Topical Reviews
Title The neglected role of insulin‐like growth factors in the maternal circulation regulating fetal growth
URI https://onlinelibrary.wiley.com/doi/abs/10.1113%2Fjphysiol.2010.198622
https://www.ncbi.nlm.nih.gov/pubmed/20921199
https://www.proquest.com/docview/1545329443
https://www.proquest.com/docview/839714473
https://pubmed.ncbi.nlm.nih.gov/PMC3021777
Volume 589
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