Maternal hyperglycaemia results in an excess maternal-foetal transfer of glucose. The placental glucose transporter protein, GLUT1, is increased in diabetic pregnancies, and maternal hyperglycaemia quickly results in foetal hyperglycaemia and foetal hyperinsulinaemia (4). Maternal hyperglycaemia is not only a critical factor in glucose-mediated congenital malformations, but also in many aspects of foetal development, neonatal well-being and future health, see Table 7.1.
An accelerated foetal growth pattern and a large-for-gestational-age (LGA) infant at birth is the hallmark of a poorly controlled diabetic pregnancy. Foetal insulin is the main foetal anabolic hormone and hyperinsulinaemia can cause excess fat accumulation, organomegaly, especially of the heart and liver, and high birthweight. An LGA infant is a potential cause for birth trauma and a high Caesarean rate. Foetal hyperinsulinaemia is also believed to contribute to adverse foetal metabolic complications in late pregnancy including a tendency to high lactate levels and an increased risk of stillbirth. Foetal hyperinsulinae-mia at delivery can cause transient hypoglycaemia and hypocalcaemia. There is increasing and tantalising evidence that by optimising maternal glycaemia and avoiding foetal hyperinsulinaemia one can reduce the long-term risk of the child becoming obese and insulin-resistant in adult life (5).
Table 7.1 The intrauterine influence of maternal hyperglycaemia on foetal and childhood development
Period of influence Consequence of maternal hyperglycaemia
First trimester Congenital malformations
Second trimester Foetal cell programming, foetal hyperinsulinaemia
Third trimester Accelerated foetal growth and stillbirth
Neonatal period Transient hypoglycaemia; hypocalcaemia and cardiomyopathy
Adolescence Obesity, impaired glucose tolerance and insulin resistance
Adulthood Insulin resistance, obesity and Type 2 diabetes
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