Frontiers in endocrinology · 2026
Adiponectin and leptin levels in mothers, fetuses, and neonates with intrauterine growth restriction compared to those with appropriate gestational age.
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Parveen Nuzhat, Iqbal Naveed, Mohamed Abdelrahim Awadelkarim Abdelrahman, Shahid Syed Monowar Alam, Abdalla Rania Abdeen Hussain, Elhussein Gamal Eldin Mohamed Osman, Azhar Mohammad Asim, Saleem Mohd, Khan Mohd Shahid
Аннотация
OBJECTIVE: Intrauterine growth restriction (IUGR) is associated with impaired fetal growth and altered metabolic regulation. Adipokines such as adiponectin and leptin play key roles in energy homeostasis and placental function. This study aimed to evaluate adiponectin and leptin levels in maternal peripheral blood, umbilical cord blood, and neonatal peripheral blood, and to investigate associated changes in placental gene expression and DNA methylation of adipokine-related genes in IUGR compared to appropriate-for-gestational-age (AGA) pregnancies.
MATERIALS AND METHODS: This case-control study included 100 IUGR and 100 AGA full-term pregnancies. Maternal peripheral blood samples were collected at delivery, umbilical cord blood immediately after birth, and neonatal peripheral blood within 24 hours postpartum. Plasma adiponectin and leptin concentrations were measured using standardized immunoassays. Placental tissue samples were analyzed for gene expression of ADIPOQ, LEP, and WFS1, along with DNA methylation profiling using established molecular techniques. Statistical analyses were performed using appropriate tests, with p < 0.05 considered significant.
RESULTS: Adipokine levels exhibited compartment-specific variations. Adiponectin levels were significantly reduced in maternal and neonatal peripheral blood in the IUGR group, while no significant difference was observed in cord blood. Leptin levels showed differential regulation: increased levels in umbilical cord blood and decreased levels in neonatal peripheral blood in IUGR, whereas maternal levels were comparable between groups. Placental analysis revealed significant downregulation of ADIPOQ and altered expression of LEP and WFS1 in IUGR. DNA methylation analysis demonstrated increased methylation of ADIPOQ and LEP genes in placental tissue, with an inverse relationship between methylation and gene expression.
CONCLUSION: IUGR is associated with distinct, compartment-specific alterations in adipokine profiles and significant epigenetic and transcriptional changes in placental tissue. These findings highlight the role of placental epigenetic regulation in adipokine signaling and emphasize the importance of tissue-specific mechanisms in the pathophysiology of fetal growth restriction.
MATERIALS AND METHODS: This case-control study included 100 IUGR and 100 AGA full-term pregnancies. Maternal peripheral blood samples were collected at delivery, umbilical cord blood immediately after birth, and neonatal peripheral blood within 24 hours postpartum. Plasma adiponectin and leptin concentrations were measured using standardized immunoassays. Placental tissue samples were analyzed for gene expression of ADIPOQ, LEP, and WFS1, along with DNA methylation profiling using established molecular techniques. Statistical analyses were performed using appropriate tests, with p < 0.05 considered significant.
RESULTS: Adipokine levels exhibited compartment-specific variations. Adiponectin levels were significantly reduced in maternal and neonatal peripheral blood in the IUGR group, while no significant difference was observed in cord blood. Leptin levels showed differential regulation: increased levels in umbilical cord blood and decreased levels in neonatal peripheral blood in IUGR, whereas maternal levels were comparable between groups. Placental analysis revealed significant downregulation of ADIPOQ and altered expression of LEP and WFS1 in IUGR. DNA methylation analysis demonstrated increased methylation of ADIPOQ and LEP genes in placental tissue, with an inverse relationship between methylation and gene expression.
CONCLUSION: IUGR is associated with distinct, compartment-specific alterations in adipokine profiles and significant epigenetic and transcriptional changes in placental tissue. These findings highlight the role of placental epigenetic regulation in adipokine signaling and emphasize the importance of tissue-specific mechanisms in the pathophysiology of fetal growth restriction.