Gestational diabetes

During pregnancy, the placenta releases human placental lactogen (HPL), which causes insulin resistance in the mother and subsequently increases serum glucose levels. This physiological adaptation ensures adequate glucose availability to meet the energy demands of both mother and developing fetus.

However, complications can arise when glucose levels become excessive. Gestational diabetes occurs when the mother's body cannot produce sufficient insulin to overcome the insulin resistance caused by HPL. This results in elevated glucose concentrations in the maternal circulation, which in turn increases glucose levels in the fetal circulation, leading to fetal hyperglycemia.

In response to this hyperglycemic environment, the fetus produces excess insulin. Since insulin functions as a growth factor, this excess production leads to macrosomia - an abnormally large fetal size that can complicate delivery.

Additionally, elevated insulin levels have another concerning effect: they inhibit surfactant production by suppressing the expression of surfactant proteins A and B (SP-A and SP-B). This inhibition increases alveolar surface tension and promotes alveolar collapse, potentially resulting in neonatal respiratory distress syndrome (also known as hyaline membrane disease).