Cause of Gestational Diabetes

During pregnancy, metabolic alterations occur within the woman’s body to meet the demand of increased energy requirements by the growing baby inside the uterus. In the initial stages of pregnancy, the level of estrogen and progesterone (a hormone secreted by the placenta) increases. These hormones bring about increase in the size of the pancreatic beta cells and facilitate the production of adequate levels of insulin to meet the growing demands. There is an increase in peripheral glucose utilization and glycogen storage with a simultaneous decrease in glucose production in the liver. All this results in low levels of fasting glucose in the pregnant woman.

The condition usually begins during  20 to 24 weeks of pregnancy.

As the pregnancy advances, increased levels of human chorionic sommatomammotropin (hCS), prolactin, progesterone, cortisol, and estrogen creates insulin resistance in the peripheral tissues. Cortisol and progesterone have high diabetogenic /anti-insulin properties.

 Expectant mothers whose pancreas is normal are able to meet the growing demands. However, those with borderline pancreatic function are unable to increase insulin production to counter the action of the other hormones. This brings about a demand for insulin which in turn results in gestational diabetes.

Resistance to insulin also result in the mother using fat for her calorie requirement as she saves the glucose for the growing baby. So extra blood glucose goes through the placenta into the growing baby and this results in high blood glucose levels in the growing baby. This results in stimulation of the baby’s pancreas to increase production of insulin and the baby receives more energy which is then stored as fat.

In addition to the above-mentioned changes, there is increased production of enzymes such as insulinase by the placenta that causes degradation of insulin.