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Published on: June 29, 2013
Placental Nutrient Transport and Intrauterine Growth Restriction
Francesca Gaccioli1, Susanne Lager1
1Department of Obstetrics and Gynaecology, University of Cambridge Cambridge, UK.
Insights
Intrauterine growth restriction (IUGR) hinders fetal growth potential, impacting millions of newborns globally. Placental nutrient transporter dysfunction is a key factor in IUGR development and lifelong health issues.
Area of Science:
- Obstetrics and Gynecology
- Fetal Medicine
- Perinatology
Background:
- Intrauterine growth restriction (IUGR) affects 5-15% of pregnancies in developed nations and up to 55% in developing countries.
- IUGR infants face high perinatal mortality and increased risks of conditions like hypoxic ischemic encephalopathy and cerebral palsy.
- Reduced fetal growth is linked to long-term health problems, including adult metabolic and cardiovascular diseases.
Purpose of the Study:
- To review alterations in placental nutrient transport in human pregnancies with intrauterine growth restriction.
- To explore the role of placental insufficiency in the etiology of IUGR.
- To summarize changes in placental amino acid, fatty acid, and glucose transport in various IUGR-associated conditions.
Main Methods:
- Literature review focusing on human pregnancies.
- Analysis of studies reporting on placental nutrient transporter expression and activity.
- Synthesis of findings related to IUGR and specific maternal conditions.
Main Results:
- Placental insufficiency is a significant contributor to intrauterine growth restriction.
- Reduced expression/activity of placental nutrient transporters is observed in IUGR.
- Specific conditions like maternal undernutrition, pre-eclampsia, and infection are associated with altered placental transport.
Conclusions:
- Dysfunctional placental nutrient transport is a critical factor in intrauterine growth restriction.
- Understanding these transport alterations is key to addressing IUGR and its long-term consequences.
- Further research into placental transport mechanisms can inform interventions for fetal growth disorders.
Abstract:
Intrauterine growth restriction refers to the inability of the fetus to reach its genetically determined potential size. Fetal growth restriction affects approximately 5-15% of all pregnancies in the United States and Europe. In developing countries the occurrence varies widely between 10 and 55%, impacting about 30 million newborns per year. Besides having high perinatal mortality rates these infants are at greater risk for severe adverse outcomes, such as hypoxic ischemic encephalopathy and cerebral palsy. Moreover, reduced fetal growth has lifelong health consequences, including higher risks of developing metabolic and cardiovascular diseases in adulthood. Numerous reports indicate placental insufficiency as one of the underlying causes leading to altered fetal growth and impaired placental capacity of delivering nutrients to the fetus has been shown to contribute to the etiology of intrauterine growth restriction. Indeed, reduced expression and/or activity of placental nutrient transporters have been demonstrated in several conditions associated with an increased risk of delivering a small or growth restricted infant. This review focuses on human pregnancies and summarizes the changes in placental amino acid, fatty acid, and glucose transport reported in conditions associated with intrauterine growth restriction, such as maternal undernutrition, pre-eclampsia, young maternal age, high altitude and infection.
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