Maintaining stable blood sugar levels during pregnancy is important for the health of both the mother and the developing baby. Expectant parents often wonder about the substances that pass between mother and fetus, especially concerning hormones like insulin.
The Placenta’s Role as a Barrier
Maternal insulin, whether naturally produced by the mother’s body or given as a medication, generally does not cross the placenta to reach the fetus. The primary reason for this is the insulin molecule’s relatively large size, which prevents it from easily passing through the placental barrier. While the placenta is designed to transfer many substances necessary for fetal development, it also acts as a selective filter, regulating what enters the fetal circulation. This selective barrier means that the fetus must manage its own glucose metabolism independently of the mother’s insulin.
How a Fetus Regulates Its Own Blood Sugar
Since maternal insulin does not readily cross the placenta, the fetus must develop its own system for managing blood sugar. Glucose, a much smaller molecule than insulin, freely crosses the placenta from the mother’s bloodstream to the baby’s. This constant supply of glucose provides the energy the growing fetus needs.
The fetal pancreas begins to develop and produce its own insulin relatively early in gestation. Insulin and glucagon, another pancreatic hormone, can be detected in the human fetal circulation by the fourth or fifth month of development, with some insulin release detectable as early as 12-15 gestational weeks. This fetal insulin is then used by the baby to process the glucose it receives from the mother’s circulation.
Effects of Maternal Blood Sugar on the Fetus
When a mother experiences high blood sugar levels, a condition known as hyperglycemia, it directly affects the fetus. Excess glucose crosses the placenta into the fetal bloodstream, leading to elevated blood sugar in the baby. This increased glucose load stimulates the fetal pancreas to produce larger amounts of its own insulin, a state called fetal hyperinsulinemia.
This excess fetal insulin acts as a growth factor, prompting the fetus to store more glucose as glycogen and fat. This can result in the baby growing significantly larger than average, a condition known as macrosomia, which increases the risk of birth complications like shoulder dystocia. After birth, when the continuous high glucose supply from the mother is suddenly cut off, the newborn’s still-elevated insulin levels can cause a rapid drop in blood sugar, leading to neonatal hypoglycemia.