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The exact pathophysiology of gestational diabetes is unknown. One main aspect of the underlying pathology is insulin resistance, where the body’s cells fail to respond to the hormone insulin in the usual way. Several pregnancy hormones are thought to disrupt the usual action of insulin as it binds to its receptor, most probably by interfering with cell signalling pathways.
Insulin is the primary hormone produced in the beta cells of the islets of Langerhans in the pancreas. Insulin is key in the regulation of the body’s blood glucose level. Insulin stimulates cells in the skeletal muscle and fat tissue to absorb glucose from the bloodstream. In the presence of insulin resistance, this uptake of blood glucose is prevented and the blood sugar level remains high. The body then compensates by producing more insulin to overcome the resistance and in gestational diabetes, the insulin production can be up to 1.5 or 2 times that seen in a normal pregnancy.
The glucose present in the blood crosses the placenta via the GLUT1 carrier to reach the fetus. If gestational diabetes is left untreated, the fetus is exposed to an excess of glucose, which leads to an increase in the amount of insulin produced by the fetus. As insulin stimulates growth, this means the baby then develops a larger body than is normal for their gestational age. Once the baby is born, the exposure to excess glucose is removed. However, the newborn still has increased insulin production, meaning they are susceptible to low blood glucose levels.
Some of the symptoms of gestational diabetes include:
Gestational diabetes raises the risk of birth complications and future health conditions. Some examples are given below: