In 3-4% of otherwise healthy pregnant women, there is no increase in insulin secretion sufficient to overcome the insulin resistance of peripheral tissues and maintain euglycemia. This condition is called gestational diabetes. Gestational diabetes is very reminiscent of type II diabetes mellitus: in both cases, increased insulin resistance of peripheral tissues and insufficient insulin secretion by the pancreas are detected. In addition, impaired glucose tolerance during pregnancy is one of the best screening tests to assess the risk of type II diabetes in the future. More than 50% of women who have had gestational diabetes during one of their pregnancies develop type II diabetes in the next 20 years. Risk factors for gestational diabetes are the presence of type II diabetes mellitus in relatives, obesity, “age-related” pregnant women, and a history of gestational diabetes. Gestational diabetes usually develops in late pregnancy, when the secretion of placental lactogen is maximal and, therefore, insulin resistance. The main complication of pregnant diabetes is fetal macrosomia due to hyperinsulinemia. With a constantly increased concentration of glucose in the blood of a pregnant woman, the fetus also develops hyperglycemia. In a fetus that is not exposed to the same high concentration of placental lactogen as a pregnant woman, insulin is formed in an amount sufficient to lower the glucose concentration. Hyperinsulinemia leads to the accumulation of nutrients in the form of fat. If the pregnant woman has diabetes mellitus, the fetus also increases the content of insulin-like growth factors 1 and 2 (somatomedins). Somatomedins affect the growth of the skeleton and internal organs and, probably, they determine the large size of the fetus in pregnant women with diabetes. Macrosomy is a clinical problem due to the fact that deliveries by a large fetus are more often accompanied by birth injuries. The size of the head increases very slightly, and it is usually born normally, however, difficulties may arise during the birth of the shoulders and trunk, which can lead to fetal asphyxiation and damage to the brachial plexus. Strict control of glucose concentration through diet and the administration of insulin if necessary helps to minimize macrosomia, but does not completely eliminate it. Obesity in a woman (in itself an independent risk factor for fetal macrosomia) further increases the risk of fetal macrosomia in pregnant women with diabetes. Pregestational diabetes mellitus The number of patients with diabetes among pregnant women is approximately 0.5%. In addition to complications associated with fetal macrosomia, hyperglycemia during embryogenesis is associated with an increased risk of congenital malformations and miscarriages. With careful monitoring of glucose concentrations during conception, the risk of diabetic embryopathy is significantly reduced, but not completely excluded. With poor glycemic control, the risk of malformations and miscarriages increases dramatically. Most often, neural tube defects and heart defects occur. The mechanism of impaired embryonic development with hyperglycemia is not fully disclosed. The type and severity of malformations indicate that they occur at the yolk sac stage, i.e. at 6-7 weeks of fetal development. The excessive formation of free radicals is probably of some importance due to the stimulating effect of excess glucose on cellular metabolism: in animal experiments, antioxidants reduce the risk of embryopathy caused by hyperglycemia. Also, apparently, there is a genetic predisposition that determines both susceptibility to damage and the damaged organ. An increase in the number of miscarriages with poor control of glycemia during pregnancy is associated with the formation of embryopathies that are not compatible with life.