Prenatal development is currently recognized as a critical period in the etiology of human diseases. This is particularly so when an unfavorable environment interacts with a genetic predisposition. The fetal programming concept suggests that maternal nutritional imbalance and metabolic disturbances may have a persistent and intergenerational effect on the health of offspring and on the risk of diseases such as obesity, diabetes, and cardiovascular diseases.

Pregnancy is a special period in a woman’s life when her organism undergoes multiple physiological changes so that the fetus has optimal conditions for growth and development. These include modifications in the composition of the microbiome that occur between the first and third trimesters of pregnancy. There is an increase in Akkermansia, Bifidobacterium, and Firmicutes, which have been associated with an increase in the need for energy storage. The growth in Proteobacteria and Actinobacteria levels has a protective effect on both the mother and the fetus via proinflammatory mechanisms. The aim of the study is to review the research on the relationship between the mother’s intestinal microbiome and gestational pathologies. Changes in the maternal gut microbiome is probably one of the mechanisms that occurs in various pregnancy diseases such as preeclampsia, fetal growth restriction, gestational diabetes mellitus, excessive gestational weight gain, and premature birth. For this reason, it seems vital to pay attention to certain interventions that can benefit the affected patients both in the short term, by preventing complications during pregnancy, and in the long term, as one of the mechanisms occurring in various gestational diseases is dysbiosis of the maternal intestinal flora.

There is ample scientific evidence to suggest a link between the fatty acid-binding protein 4 (FABP4) and insulin resistance, gestational (GDM), and type 2 (T2DM) diabetes mellitus. This novel proinflammatory adipokine is engaged in the regulation of lipid metabolism at the cellular level. The molecule takes part in lipid oxidation, the regulation of transcription as well as the synthesis of membranes. An involvement of FABP4 in the pathogenesis of obesity and insulin resistance seems to be mediated via FABP4-dependent peroxisome proliferator-activated receptor γ (PPARγ) inhibition. A considerable number of studies have shown that plasma concentrations of FABP4 is increased in obesity and T2DM, and that circulating FABP4 levels are correlated with certain clinical parameters, such as body mass index, insulin resistance, and dyslipidemia. Since plasma-circulating FABP4 has the potential to modulate the function of several types of cells, it appears to be of extreme interest to try to develop potential therapeutic strategies targeting the pathogenesis of metabolic diseases in this respect. In this manuscript, representing a detailed review of the literature on FABP4 and the abovementioned metabolic disorders, various mechanisms of the interaction of FABP4 with insulin signaling pathways are thoroughly discussed. Clinical aspects of insulin resistance in diabetic patients, including women diagnosed with GDM, are analyzed as well.

There is growing evidence of long-term cardiovascular sequelae in children after in utero exposure to preeclampsia. Maternal hypertension and/or placental ischaemia during pregnancy increase the risk of hypertension, stroke, diabetes, and cardiovascular disease (CVD) in the offspring later in life. The mechanisms associated with CVD seem to be a combination of genetic, molecular, and environmental factors which can be defined as fetal and postnatal programming. The aim of this paper is to discuss the relationship between pregnancy complicated by preeclampsia and possibility of CVD in the offspring. Unfortunately, due to its multifactorial nature, a clear dependency mechanism between preeclampsia and CVD is difficult to establish.

The fetus may be exposed to increased endogenous or synthetic glucocorticoid (GS) exposure in late gestation. Approximately 7% of pregnant women in Europe and North America are treated with synthetic GSs to promote lung maturation in fetuses at risk of preterm delivery. Maternal steroid treatment before preterm delivery is one of the best documented and most cost effective life saving treatments in prenatal medicine but, in certain circumstances, the price of accelerated lung maturity may be loss of brain cells, increased neurodevelopmental disability, intra-uterine growth restriction (IUGR), and an increased risk of preterm delivery, of programming of post-natal hypertension, and of increased postnatal activity in the hypothalamo-pituitary-adrenal (HPA) axis. Placental 11β-hydroxysteroid dehydrogenase type 2 (11β- HSD2) is the key enzyme which protects the fetus from overexposure to GSs by their oxidation into inactive derivates. We review the evidence for the metabolism of GSs during pregnancy and how endogenous and synthetic GSs cause other changes in the placenta which affect fetal development.

Endometriosis is a disease that affects women of reproductive age and has a significantly negative impact on their well-being. The main symptoms are dysmenorrhoea, chronic pelvic pain and infertility. In many patients the diagnostic process is very long and can take up to 8–12 years. Laparoscopy, an invasive method, is still necessary to confirm the diagnosis. Therefore, development of more effective diagnostic markers appears to be of the utmost importance for early diagnosis of endometriosis and provision of appropriate treatment. From a clinical point of view, detection of early-stage endometriosis in asymptomatic patients is an ideal situation since early diagnosis of endometriosis may delay the onset of symptoms as well as prevent progression and complications. In the meantime, Cancer Antigen 125 (CA-125) is still the most frequently studied and used marker. Other glycoproteins, growth factors and immune markers seem to play an important role. However, the search for an ideal endometriosis marker is still underway. Further studies into the pathogenesis of endometriosis will help to identify biomarkers or sets of biomarkers with the potential to improve and speed up the diagnostic process in a non-invasive way.