Ebook Components Of Metabolic Syndrome And Their Impact On Fetal Growth In Women With Gestational Diabetes Mellitus
Pregnancy is commonly recognized as a state of physiological, and temporary insulin resistance. This condition is driven by high concentrations of steroid hormones such as progesterone, estrogens, prolactin, cortisol and by placenta derived human placental lactogen all of them having a diabetogenic action combined with a decreased sensitivity of insulin receptors within target tissues. The main reason for all these changes is to provide a preferential supply of nutrients (mainly glucose) to the fetus. Usually, in maternal compartment low levels of glucose (even lower than these in non-pregnant women) are maintained due to increased maternal production of insulin and accelerated “drainage” of glucose by uteroplacental unit to cover fetal needs (“accelerated starvation”). However, in some percentage of pregnant population (3% up to 9%, according to population and diagnostic methods) a transient form of glucose intolerance develops if a degree of gestational insulin resistance is beyond the compensatory capability of the pancreas.
Gestational diabetes mellitus (GDM) is defined as a glucose intolerance of any degree diagnosed or first recognized during pregnancy. In most of the cases it is a gestation-related disease and patient’s normal carbohydrates metabolism is restored within a couple of weeks after a delivery. However, a GDM-complicated pregnancy is still associated with a high perinatal risk with increased neonatal mortality and morbidity, mainly as a result of fetal macrosomia as well as operative and instrumental deliveries, birth trauma and metabolic abnormalities in newborn. In this group of pregnant women there is still increased incidence of intrauterine fetal death in term pregnancy. Moreover, a history of gestational diabetes is a strong risk factor for serious maternal complications in later life, including metabolic syndrome, type 2 diabetes and cardiovascular diseases that are considered a leading cause of death in the female population.
The major reason for poor perinatal outcome is fetal macrosomia (defined as large for gestational age, with a birth weight above the 90th percentile; LGA). Fetal overgrowth induced by fetal hyperinsulinemia can develop as a response to increased placental glucose transfer to the fetus which is secondary to maternal hyperglycemia. Fetal hyperinsulinemia and accelerated fetal growth is also associated with a cluster of abnormalities usually referred to as “diabetic fetopathy” that may be grounds for serious neonatal complications, including hypoglycemia and respiratory distress.
In recent decades, significant improvements in perinatal care, diagnostic and treatment of GDM complicated pregnancies has been made. Despite that, macrosomia still remains a serious problem, which may complicate up to 30% of diabetic pregnancies. Interestingly, the certain percentage of newborns with macrosomia remains high even in women with proper carbohydrate controls, measured using commonly available parameters (fasting and 2-hrs postprandial glycemia, HbA1c concentration). Therefore, further studies are necessary to investigate other factors contributing to fetal overgrowth in diabetic pregnancy. Maternal hyperglycemia is a commonly recognized classical risk factor for fetal overgrowth. However, it is still debatable whether fasting or postprandial hyperglycemia is a pivotal factor for developing fetal overgrowth.
In recent studies fetal growth and development is considered a complex process where maternal characteristics, fetal potential and the intrauterine environment plays an important role. This concept opens a new horizon for further research; however, there are a limited number of tools and techniques designed for investigating fetal development and the intrauterine milieu. Moreover, the list of factors influencing fetal growth both in normal and in diabetic pregnancy is expanding and still far from being complete, results of different studies are often conflicted and new areas for research emerge.
Recently, a great deal of data has accumulated on lipid metabolism in normal and diabetic pregnancies, maternal obesity and gestational insulin resistance, however, data concerning their impact on fetal growth are limited.
Pregnancy is commonly described as a condition characterized by a rapid increase in all lipids, however, evidence concerning the relationship between lipid metabolism and hormonal changes during fetal gestation is conflicting. In the study performed on a small group of 9 women with GDM, Montelongo et al. reported a linear correlation between HDL-cholesterol, TAG and ?-estradiol, progesterone and prolactin a finding supported only for TAG by more recent study performed on a larger group by Smolarczyk et al.. In their study, Knopp et al. reported a significant association between maternal triglyceride levels and neonatal weight both in normal and in GDM-complicated pregnancy. Their results were in line with those obtained by Kitaima et al. who reported maternal hypertriglyceridemia as a significant predictor of LGA.
In our study we aim to investigate different maternal metabolic characteristics corresponding to particular features of metabolic syndrome and their compounding influence on fetal growth and the incidence of LGA in pregnant women with GDM.
Posted in :
