Recommendations for weight gain during pregnancy are based on pre-pregnancy body mass index (BMI). Pregnancy is a risk factor for excessive weight gain and many endocrine problems, making it difficult to return to pre-pregnancy weight and increasing the risk of postpartum obesity and, consequently, type 2 diabetes and metabolic syndrome. Both excessive gestational weight gain (EGWG) and obesity are associated with an increased risk of gestational hypertension, pre-eclampsia, gestational diabetes, cesarean section, shoulder dystocia, and neonatal macrosomia. In the long term, EGWG is associated with increased morbidity and mortality, particularly from diabetes, cardiovascular disorders, and some cancers. This study aims to present recommendations from various societies regarding weight gain during pregnancy, dietary guidance, and physical activity. In addition, we discuss the pathophysiology of this complication and the differential diagnosis in pregnant women with EGWG. According to our research, inadequate nutrition might contribute more significantly to the development of EGWG than insufficient physical activity levels in pregnant women. Telehealth systems seem to be a promising direction for future EGWG prevention by motivating women to exercise. Although the importance of adequate pre-pregnancy weight and weight gain during pregnancy is well known, an increasing number of women gain excessive weight during pregnancy.

Bioelectrical impedance analysis (BIA) has a wide range of applications. For over 25 years, it has primarily been utilized for assessing body composition. This method is non-invasive, portable, widely available, cost-effective, and user-friendly, offering the advantage of repeatability and minimal dependence on patient cooperation. BIA measures the impedance of the whole body, specifically the body’s resistance to alternating current. In postpartum women, who undergo significant physiological changes following childbirth, BIA can serve as a valuable diagnostic and monitoring tool. It is commonly employed to track body weight and fat reduction, and it facilitates the differentiation of fat mass, muscle mass, and body water content. This enables the customization of nutritional plans and the development of individualized training regimens tailored to the patient’s health status. Additionally, BIA aids in the assessment of hydration status, which is particularly critical during the postpartum period when women often experience fluid retention. Furthermore, optimal hydration is essential for lactation and maintaining favorable conditions for breastfeeding. BIA is also invaluable for evaluating nutritional status, micronutrient balance, and preventing both overweight and malnutrition. Moreover, BIA supports physical recovery by monitoring muscle mass, thereby assisting in the assessment of pelvic floor muscle regeneration following childbirth.

Congenital metabolic disorders often lead to irreversible organ damage beginning during fetal life or shortly after birth. Advances in prenatal diagnostics have enabled earlier identification of these conditions, creating opportunities for prenatal therapeutic intervention. Preclinical studies have demonstrated that prenatal cell therapies can result in donor cell engraftment, enzyme production, and partial correction of metabolic defects in several disease models. The fetal environment may support immune tolerance and enhance treatment effectiveness. Limited clinical experience suggests that these approaches are feasible and may be beneficial in selected conditions, including lysosomal storage diseases and infantile-onset Pompe disease. In utero gene therapy has also shown long-term metabolic correction in animal models. However, important challenges remain, including limited engraftment, immune responses, vector safety, ethical concerns, and regulatory barriers. Prenatal cellular and gene-based therapies are promising but remain experimental. Current evidence is strongest for biological rationale and preclinical proof of concept; clinical benefit has not yet been established for most disorders. Further clinical studies are needed to determine their safety, efficacy, and future role in the treatment of congenital metabolic disorders. This article reviews the current status of prenatal fetal cellular and gene‑based therapeutic approaches for inborn errors of metabolism.

Preterm labor is a leading cause of neonatal morbidity and mortality, with inflammation playing a central role in its pathogenesis. This structured literature review summarizes the role of the nuclear factor kappa B (NF-κB) signaling pathway in term and preterm labor and critically evaluates current evidence on natural and synthetic NF-κB modulators as potential therapeutic approaches. The narrative overview covers publications through June 2026. Experimental, translational, and review studies were synthesized narratively. NF-κB integrates hormonal, mechanical, infectious, and sterile inflammatory signals in gestational tissues, promoting the expression of pro-inflammatory cytokines, cyclooxygenase-2, prostaglandins, chemokines, and contraction-associated proteins that drive uterine activation. While tightly regulated NF-κB activation is essential for physiological term labor, it’s premature or excessive activation contributes to inflammation-associated preterm labor. Natural compounds and synthetic agents consistently attenuate excessive NF-κB signaling and downstream inflammatory responses in preclinical models, supporting their potential as candidate therapeutic strategies. However, clinical evidence remains limited. Future research should prioritize tissue-specific, context-dependent modulation of NF-κB and establish the safety, optimal therapeutic windows, and clinical efficacy of NF-κB-targeted interventions during pregnancy.

Preterm labor is a leading cause of neonatal morbidity and mortality, with inflammation playing a central role in its pathogenesis. This structured literature review summarizes the role of the nuclear factor kappa B (NF-κB) signaling pathway in term and preterm labor and critically evaluates current evidence on natural and synthetic NF-κB modulators as potential therapeutic approaches. To ensure comprehensive identification of relevant studies, a structured literature search informed by PRISMA 2020 reporting recommendations was performed, including studies published through August 2025. Experimental, translational, and review studies were synthesized narratively. NF-κB integrates hormonal, mechanical, infectious, and sterile inflammatory signals in gestational tissues, promoting the expression of pro-inflammatory cytokines, cyclooxygenase-2, prostaglandins, chemokines, and contraction-associated proteins that drive uterine activation. While tightly regulated NF-κB activation is essential for physiological term labor, its premature or excessive activation contributes to inflammation-associated preterm labor. Natural compounds and synthetic agents consistently attenuate excessive NF-κB signaling and downstream inflammatory responses in preclinical models, supporting their potential as candidate therapeutic strategies. However, clinical evidence remains limited. Future research should prioritize tissue-specific, context-dependent modulation of NF-κB and establish the safety, optimal therapeutic windows, and clinical efficacy of NF-κB-targeted interventions during pregnancy.

Pregnancy is a physiological state of transient, reversible insulin resistance accompanied by major adaptations in glucose and lipid metabolism. Although placental hormones are key drivers of gestational insulin resistance, the mechanisms underlying the rapid restoration of insulin sensitivity after delivery remain incompletely understood. This review proposes a conceptual framework in which fibroblast growth factor 21 (FGF21) and sex hormone-binding globulin (SHBG) are considered as complementary hepatic signals potentially involved in maternal metabolic adaptation. During late pregnancy, FGF21 may function as a metabolic stress-response factor associated with fatty acid oxidation, lipid handling, and mitochondrial adaptation through AMPK–PPARα-related pathways. Reduced SHBG, in contrast, may reflect hepatic insulin resistance and altered hepatic metabolic regulation. After delivery, changes in FGF21 and SHBG levels may be associated with recovery of hepatic metabolic homeostasis and insulin sensitivity, while persistent adaptive FGF21 signaling facilitate metabolic reprogramming may contribute to ongoing metabolic adaptation. Postpartum metabolic recovery may therefore represent an active and dynamic process rather than a purely passive consequence of placental hormone withdrawal. Disruption of FGF21- and SHBG-mediated pathways may contribute to persistent insulin resistance and increased cardiometabolic risk after gestational diabetes. Understanding hepatokine-mediated regulation of maternal metabolic flexibility may provide further insight into postpartum metabolic recovery and may support future development of risk stratification strategies, biomarker-based approaches, and preventive interventions aimed at reducing the risk of type 2 diabetes after pregnancy.