Why do babies of diabetic mothers develop hypoglycaemia after birth?

In utero, maternal hyperglycaemia drives fetal hyperglycaemia, causing hyperplasia of the fetal pancreatic islets of Langerhans and fetal hyperinsulinaemia.

At birth the maternal glucose supply is suddenly cut off, but the baby's insulin remains high, so glucose is rapidly consumed and neonatal hypoglycaemia develops in the first hours of life.

Clinical relevance. The islet-hyperplasia/hyperinsulinaemia mechanism is the examined explanation for IDM hypoglycaemia and macrosomia.

More Detail

Neonatal hypoglycaemia in the IDM

This is a direct consequence of the fetal response to maternal hyperglycaemia.

Mechanism

1. Maternal hyperglycaemia -> glucose crosses the placenta -> fetal hyperglycaemia.
2. The fetal pancreas responds with hyperplasia of the islets of Langerhans and hyperinsulinaemia (insulin does not cross the placenta, so the fetus makes its own).
3. At birth, the maternal glucose supply abruptly stops, but the neonatal insulin level stays high.
4. The mismatch causes glucose to be consumed rapidly -> neonatal hypoglycaemia in the first hours.

Implications

• Maternal glycaemic control during labour and birth reduces fetal hyperinsulinaemia at delivery.
• Early and frequent breastfeeding with pre-feed glucose monitoring prevents and detects hypoglycaemia.

The same hyperinsulinaemia also drives macrosomia antenatally.