Nutritional modulation of adolescent pregnancy outcome -- a review.
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.
Wallace
J M
JM
Development, Growth and Function Division, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, UK. jacqueline.wallace@rri.sari.ac.uk
Luther
J S
JS
Milne
J S
JS
Aitken
R P
RP
Redmer
D A
DA
Reynolds
L P
LP
Hay
W W
WW
D000293:Adolescent; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation; D006801:Humans; D044342:Malnutrition; D039382:Maternal Nutritional Physiological Phenomena; D023421:Models, Animal; D010920:Placenta / Q000098:blood supply / Q000502:physiology; D011247:Pregnancy; D011256:Pregnancy Outcome; D011253:Pregnancy in Adolescence / Q000502:physiology*; D012756:Sheep; D012919:Social Behavior; D014599:Uterus / Q000098:blood supply