Glucose metabolism in early pregnancy is characterized by hypoglycemia, hypoinsulinemia, ketogenesis, and fatty acid turnover. Between 24–28 weeks of gestation, the concentrations of placental and insulin-antagonistic factors increase, altering carbohydrate metabolism. This is interpreted as antagonism of the action of circulating insulin. Due to the reaction of the pancreas, insulin secretion increases. However, in some cases, the reserves of the pancreas can be reduced or depleted [6]. Due to the abnormal metabolism of carbohydrates, altered maternal glucose homeostasis develops, which is a condition referred to as DMG. The basis of the disorder is increased secretion of hPL (although growth hormone is reduced), as well as the effect of placental insulinases [7].

Insulin degradation on the maternal side of the placenta is unilateral, since insulin does not cross the placental barrier. The insulin resistance is of the post-receptor type and is hormonally conditioned. A decrease in the number of insulin receptors bound to peripheral target cells, along with a relative lack of circulating insulin, including post-receptor defects, leads to glucose intolerance and the development of gestational diabetes [8,9].

Changes in the mother’s glucose and insulin concentrations are followed by similar changes in the fetus. Maternal hyperglycemia leads to fetal hyperglycemia and hyperinsulinemia. The consequences of this excessive stimulation are reflected in the fetal pancreas in the form of islet hyperplasia with an increase in the number of beta cells and increased insulin values [10]. The importance of detecting gestational diabetes in the early stages of pregnancy is best illustrated by the data reporting a significant percentage of morbidity and mortality in newborns, in mothers in whom this disorder is undiagnosed and untreated, and in those when it is discovered late in pregnancy [11]. Fetal adiposity, which is also found in well-regulated diabetes, is explained by an increase in free fatty acids in the placenta, with increases the transfer to the fetus. The passage of amino acids through the placenta regulates insulin (hyperinsulinemia increases the transfer), and the fetal pancreas responds to an increase in the concentration of amino acids and glucose by producing insulin [12]. This is one of the important reasons for the occurrence of fetal macrosomia. It was found that the concentration of amino acids is higher in the fetal circulation than in the maternal circulation, while fetal glycemia is approximately 1.1–1.6 mmol/L lower than the maternal glycemia, i.e., 70–80% of maternal glycemia [13]. Medical nutritional therapy is the first-line approach in managing gestational diabetes mellitus (GDM). Diet is also a powerful modulator of the gut microbiota, whose impact on insulin resistance and the inflammatory response in the host are well known. Changes in the gut microbiota composition have been described in pregnancies either before the onset of GDM or after its diagnosis. The possible modulation of the gut microbiota by dietary interventions in pregnancy is a topic of emerging interest, in consideration of the potential effects on maternal and consequently neonatal health. To date, very few data from observational studies are available about the associations between diet and the gut microbiota in pregnancy complicated by GDM. In this review, we analyzed the available data and discussed the current knowledge about diet manipulation in order to shape the gut microbiota in pregnancy [14].

The priority of current studies is to discover mechanisms by which epigenetic modification prolongs the effects of environmental influences in early childhood and provides a long-lasting response to transient stimulus-modified gene expression and phenotype in adults [15].

Thus, nutrition in the pre- and postnatal period positively influences health in adulthood [16]. An adverse intrauterine environment in pregnancy complicated with diabetes has long-term consequences for the offspring because of the effects of epigenetics [17]. Optimal control of pregnant women’s glycemia can reduce the adverse consequences of pregnancy complicated with diabetes because the glucose level and perinatal outcome are a continuum [18]. Children of mothers with GDM are at greater risk of obesity, diabetes type 1 and 2, hypertension, lipid changes, and albuminuria in preadolescent age and in adulthood [19]. Mental and motor deficits as well as attention and behavioral disorders are much more common in the offspring of mothers with diabetes [20,21]. Many consequences of GDM during pregnancy can be prevented. Early breastfeeding can prevent metabolic complications in neonates because colostrum is rich in glucose, and hypoglycemia may be asymptomatic. GDM can lead to not only development of fetal macrosomia, neonatal hypoglycemia, jaundice, polycythemia, and hypocalcemia during the perinatal period, but also childhood obesity and metabolic syndrome in adulthood [22].

3. Gestational Diabetes Mellitus and Meconium Microbiota