Intrauterine growth restriction (IUGR) is increasingly recognized as a condition with profound implications for fetal metabolic programming, predisposing individuals to insulin resistance, obesity, and cardiovascular disease in adulthood. Central to this process are adipocytokines—bioactive molecules secreted by adipose tissue that regulate energy homeostasis, inflammation, and insulin sensitivity. Among these, adiponectin and leptin play opposing roles: adiponectin exerts anti-inflammatory and insulin-sensitizing effects, while leptin primarily regulates appetite and energy balance but also contributes to immune activation and endothelial dysfunction when dysregulated. This study investigates the maternal-fetal serum levels of adiponectin and leptin in IUGR, small-for-gestational-age (SGA), and appropriate-for-gestational-age (AGA) pregnancies, aiming to clarify their role in metabolic and vascular adaptation during fetal development.
A retrospective cohort analysis was conducted on 140 pregnant women from the University of Padua between January 2011 and March 2013. Participants were stratified into three groups: 37 IUGR (EFW < 10th percentile with abnormal umbilical artery Doppler), 33 SGA (EFW < 10th percentile without Doppler abnormalities), and 70 AGA (EFW ≥ 10th percentile). Blood samples were collected at delivery from both mothers and umbilical cords. Serum concentrations of adiponectin and leptin were measured using radioimmunoassay kits with high analytical precision. Adiponectin levels were determined via Millipore RIA kit (HADP-61HK), with a sensitivity of 1 μg/L and measuring range of 1–240 μg/L. Leptin was assessed using Mediagnost’s streptavidin-coated tube assay, with sensitivity of 0.1 μg/L and a dynamic range of 0.1–64 μg/L. Results revealed a striking imbalance in adipocytokine profiles among IUGR fetuses. Fetal adiponectin levels were significantly lower in IUGR compared to both SGA (p < 0.05) and AGA (p < 0.05) groups, with median values of 134 μg/L versus 197 μg/L and 196 μg/L, respectively. Conversely, fetal leptin levels were markedly elevated in IUGR fetuses (median 7.1 μg/L) compared to SGA (4.3 μg/L) and AGA (4.9 μg/L) (p < 0.05). The adiponectin-to-leptin ratio (A/L ratio), considered a key indicator of metabolic risk, was significantly reduced in IUGR fetuses (median 17.4) compared to SGA (43.5) and AGA (41.3) (p < 0.05). Maternal findings mirrored those in the fetus. Maternal adiponectin was significantly lower in IUGR women (median 45 μg/L) than in SGA (58 μg/L) and AGA (57 μg/L) (p < 0.05). Maternal leptin was highest in IUGR (8.2 μg/L), followed by SGA (8.5 μg/L), and lowest in AGA (5.5 μg/L) (p < 0.05). These results suggest a systemic shift toward a pro-inflammatory and metabolically unfavorable state in IUGR pregnancies. Correlation analyses demonstrated that fetal adiponectin positively correlated with gestational age at delivery (p < 0.05) and birth weight (p < 0.05), indicating its physiological importance in normal fetal development.Triisopropyl Autophagy In contrast, fetal leptin showed a positive correlation with aIMT (p < 0.BCL6 Antibody In Vitro 05), suggesting a direct link between increased leptin and vascular remodeling.PMID:35155866 Furthermore, the A/L ratio exhibited a significant negative correlation with aIMT in IUGR fetuses (p < 0.05), reinforcing the hypothesis that an imbalance between adiponectin and leptin may drive early atherosclerotic changes. The pathophysiological mechanisms underlying these findings involve multiple pathways. Reduced adiponectin impairs insulin signaling and promotes inflammation by failing to suppress macrophage activation and cytokine release. Elevated leptin contributes to oxidative stress, endothelial dysfunction, and increased vascular tone. Together, they create a permissive environment for vascular damage, even in the absence of overt hyperglycemia or hypertension. These results highlight the critical role of adipocytokine dysregulation in the developmental origins of health and disease. The observed imbalance in adiponectin and leptin in IUGR fetuses may represent an adaptive response to nutrient scarcity, but one that carries long-term risks. Early identification of this profile could enable targeted interventions, such as maternal nutritional optimization or postnatal monitoring of metabolic parameters, to mitigate future disease burden. In conclusion, IUGR is associated with a distinct adipocytokine signature characterized by low adiponectin, high leptin, and a reduced A/L ratio. This imbalance correlates with increased vascular thickness and systemic inflammation, suggesting a mechanistic link between fetal metabolic programming and adult-onset cardiovascular disease. Future research should explore whether modulating this axis during pregnancy can improve long-term outcomes for affected offspring.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com