Document Detail


Nutritional modulation of adolescent pregnancy outcome -- a review.
MedLine Citation:
PMID:  16442614     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The risks of miscarriage, prematurity and low birth weight are particularly acute in adolescent girls who are still growing at the time of conception. The role of maternal nutrition in mediating pregnancy outcome in this vulnerable group has been examined in sheep models. When singleton bearing adolescent dams are overnourished to promote rapid maternal growth throughout pregnancy, growth of both the placenta and fetus is impaired, and birth occurs prematurely relative to control adolescents of equivalent age. Studies at mid-gestation, prior to alterations in placental mass, suggest that reduced proliferation of the fetal trophectoderm, impaired angiogenesis, and attenuated uteroplacental blood flows are early defects in placental development. By late pregnancy, relative placental mass is reduced by 45% but uteroplacental metabolism and placental glucose transfer capacity remain normal when expressed on a placental weight specific basis. The asymmetrically growth-restricted fetuses are hypoxic, hypoglycemic and have reduced insulin and IGF-1 concentrations. Absolute umbilical nutrient uptakes are attenuated but fetal utilisation of glucose, oxygen and amino acids remains normal on a fetal weight basis. This suggests altered sensitivities to metabolic signals and may have implications for subsequent metabolic health. At the other end of the nutritional spectrum, many girls who become pregnant have inadequate or marginal nutritional status during pregnancy. This situation is replicated in a second model whereby dams are prevented from growing during pregnancy by relatively underfeeding. Limiting maternal intake in this way gradually depletes maternal body reserves leading to a lower transplacental glucose gradient and a modest slowing of fetal growth in late pregnancy. These changes appear to be independent of alterations in placental growth per se. Thus, while the underlying mechanisms differ, maternal intake at both ends of the nutritional spectrum is a powerful determinant of fetal growth in pregnant adolescents.
Authors:
J M Wallace; J S Luther; J S Milne; R P Aitken; D A Redmer; L P Reynolds; W W Hay
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2006-01-25
Journal Detail:
Title:  Placenta     Volume:  27 Suppl A     ISSN:  0143-4004     ISO Abbreviation:  Placenta     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-04-18     Completed Date:  2006-09-26     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  S61-8     Citation Subset:  IM    
Affiliation:
Development, Growth and Function Division, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, UK. jacqueline.wallace@rri.sari.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Animal Nutritional Physiological Phenomena
Animals
Female
Fetal Development*
Fetal Growth Retardation
Humans
Malnutrition
Maternal Nutritional Physiological Phenomena*
Models, Animal
Placenta / blood supply,  physiology
Pregnancy
Pregnancy Outcome*
Pregnancy in Adolescence / physiology*
Sheep
Social Behavior
Uterus / blood supply
Grant Support
ID/Acronym/Agency:
DK52138/DK/NIDDK NIH HHS; HD20764/HD/NICHD NIH HHS; HD45784/HD/NICHD NIH HHS; HL64141/HL/NHLBI NIH HHS

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