Obesity in women is an important element that determines the health of a future mother and her newborn baby [1]. A commonly used definition of obesity was proposed by the WHO in 1997 [2]. It is described as a condition characterized by an increase in body weight through hypertrophy and/or hyperplasia of adipose tissue, above 25% of the proper body weight in men and over 30% in women, posing a health risk [3]. One of the most frequently used weight indicators is Quetelet II, more commonly known as the Body Mass Index (BMI). It is calculated according to the following formula: body weight [kg]/(height [m²]). Overweight is defined as a BMI of 25 to 29.9, and obesity is defined as a BMI of 30 kg/m² or higher [4]. The pathogenesis of obesity is complex, where genetic, environmental, social, cultural, metabolic, and endocrine factors play equal roles [5]. It has been proven that the excessive bodyweight of one of the parents increases the risk of obesity in a child by four–five times, and obesity of both of parents can even increase the risk by thirteen times [6].

The risk of obstetric complications, especially in the perinatal period, increases with the mother’s BMI by increasing the number of cesarean sections and surgical deliveries, gestational diabetes, and large for gestational age neonates [7,8]. Maternal obesity may also cause later health problems for the child, including the risk of obesity in the preschool age. The literature suggests that not only obesity itself, but also excessive weight gain especially in the third trimester of pregnancy, increases the frequency of these complications—particularly in the cases of overweight and obese women diagnosed before pregnancy [9]. Su et al. revealed that macrosomic newborns are born almost exclusively to obese mothers or mothers with excessive weight gain during pregnancy [10]. A similar tendency was also observed in the conducted studies, confirming the occurrence of macrosomia in 35% of newborns in pre-pregnancy obese women and only in 7.4% of children of mothers with lower body weight.

Obesity causes regulatory disturbances in many metabolic pathways including carbohydrate metabolism, and especially insulin. Obese women have higher serum levels of this hormone compared with those with lower body weight [11,12]. The literature indicates that it is mainly due to a chronic subclinical inflammatory process occurring systemically, especially in insulin-sensitive tissues, including skeletal muscle and adipose tissue [13]. However, it should not be forgotten that the increase in insulin concentration in a pregnant woman and the intensification of insulin resistance are a physiological change during pregnancy, ensuring the proper delivery of nutrients to the fetus [11,12].

The theory of “intrauterine programming” assumes that some features, such as the intrauterine environment or genetic factors, can affect the ability of the maternal-placental transport of substances responsible for the growth and development of the fetus [14]. Pre-pregnant obesity also increases the risk of developing diseases later in life, especially type 2 diabetes [7,15,16]. It has been found that newborns of obese mothers, in addition to the above-mentioned macrosomia, are at greater risk of developing many other complications, such as prematurity, periventricular leukomalacia, and birth defects. Moreover, these children more often achieve lower Apgar scores [7,17].

During the pregnancy, there are changes in the lipid metabolism caused by the response to the increased concentration of estrogens and progesterone. The HDL and LDL lipoprotein fractions responsible for the transport of cholesterol cause the accumulation of adipose tissue, and reduced lipolysis increases the risk of obesity [18]. Lipid metabolism at the beginning of pregnancy has an anabolic effect via accumulating energy. Catabolism prevailing in the third trimester generates substrates for the developing fetus. Dyslipidemia disorder during pregnancy causes complications for the woman, the fetus, and also for the newborn [19,20]. Similarly, disturbances in carbohydrate metabolism caused by hyperinsulinism, physiological insulin resistance, and increased levels of cortisol and placental lactogen significantly mobilize adipose tissue [21]. To sum up, pre-pregnancy obesity in women is one of the most important obstetric problems, increasing the risk of both maternal and fetal complications [22].

The adipose tissue serves as an energy store, thermal insulation and protection, and also as an endocrine organ, delivering biologically active substances with hormonal properties called adipokines to the bloodstream.

The brain, stomach, breast gland, and placenta release leptin in modest levels 2–3 h after a meal [23]. Blocking neuropeptide Y and suppressing hunger, it regulates appetite. Gluconeogenesis intensifies glucose metabolism, energy utilization, tissue insulin sensitivity and secretion, blood pressure, and angiogenesis [24]. The serum leptin concentration is principally affected by adipose tissue, insulin, glucose, glucocorticosteroids, and TNF-α [25,26]. Leptin is increased in healthy pregnant women’s blood serum [27]. Its serum concentration peaks in the second trimester and lasts until delivery. The placenta produces leptin throughout pregnancy [28].

Only adipose tissue secretes adiponectin, a protein with anti-inflammatory, anti-atherosclerotic, and anti-diabetic effects. This hormone prevents atherosclerosis, obesity, and insulin resistance by promoting insulin secretion, tissue insulin sensitivity, muscle glucose uptake, inflammation reduction, and lipid reduction. Healthy adults have 5–30 μg/mL of it in their blood serum, but obese people have less [29]. Adiponectin concentration increases in the first trimester due to nutrient storage, then declines by 60% in the second half [30]. Obese pregnant women have decreased adiponectin levels [31]. Umbilical cord blood contains four–seven times more than birthing blood serum [32]. Adiponectin production by the human placenta is contradictory [33,34]. It may regulate placental nutrition transfer to regulate fetal growth [31,35].

Resistin increases liver gluconeogenesis to maintain blood glucose [36]. This cytokine inhibits isolated fat cell insulin-stimulated glucose absorption, which may increase hepatic insulin resistance. Low resistin levels may increase insulin sensitivity and de-crease induced hyperglycemia. These findings implicate resistin in diabetes and obesity [37]. Human monocytes and macrophages generate resistin, with adipocytes producing less [38,39,40]. Human plasma resistin ranges from 7 to 22 ng/mL and is favorably linked with fat tissue [29]. The placenta secretes resistin, which may help the developing embryo have enough energy [40]. This may explain its relationship with infant weight [41].

TNF-α’s anticancer and immunomodulatory properties contribute to the development of many illnesses, notably those with an inflammatory background [42,43]. This cytokine was found to regulate body weight in adipose tissue in the early 1990s. Obese people had greater serum TNF-α levels, proportional to their adiposity. Short-term TNF-α exposure inhibited adipose tissue development [44]. However, increased body fat develops TNF-α resistance [45]. TNF-α concentration and receptor affinity may explain the role of this cytokine in obesity pathophysiology. TNF-α is a therapeutic target for inflammatory illnesses such as rheumatoid arthritis, Crohn’s disease, atherosclerosis, sepsis, and obesity [46]. In the third trimester, serum TNF-α concentrations peak [47]. Maternal, fetal, and placental macrophages release TNF-α throughout this time. Many studies have linked pregnancy complications such as preterm fetal bladder rupture, hypertension, and intrauterine growth restriction to increased serum TNF-α levels [47,48].