The reduced fetal growth in intrauterine growth restriction (IUGR) has been attributed to decreased placental blood flow whereas maternal hyperglycemia is believed to represent the primary cause of accelerated fetal growth in pregnancies complicated by diabetes. However, recent research has demonstrated specific changes in placental transport function in association to these pregnancy complications that are likely to contribute to the altered fetal growth patterns. For example, in IUGR the activity of certain key amino acid transporters is reduced in the placental barrier and accelerated fetal growth in diabetes is associated with an increased activity of placental glucose and amino acid transporters. Therefore, placental insufficiency in IUGR is not just a question of reduced placental blood flow and up-regulation of placental nutrient transporters in diabetes may explain the high incidence of accelerated fetal growth despite rigorous maternal glycemic control.
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