ATP Quantification in Placental Tissue of Women Affected by Maternal Obesity and Gestational Diabetes Mellitus

Introduction: Maternal obesity (MO) and Gestational Diabetes Mellitus (GDM) represent risk factors for both mother and child short/long term consequences. The placental energy homeostasis is fundamental for a positive pregnancy outcome. Adenosine TriPhosphate (ATP), produced by the mitochondria, has a central role in cell energy balance and signaling. Placental mitochondria are reported to be altered in MO and GDM, but little is known about their capacity to produce ATP.Here we assessed placental ATP levels in healthy obese (OB) and obese with GDM (OB+GDM) vs normal weight (NW) mothers. Methods: Placental villous tissue was collected at elective caesarean section of 35 Caucasian women with singleton pregnancies: 12 NW, 15 OB, 8 OB+GDM. ATP content was determined by CellTiter-Glo Luminescent Cell Viability Assay, appropriately adapted to placental tissue. Results: One-Way ANOVA (GraphPad Prism) showed significant diff erences in placental ATP levels (p<0.001). Tukey’s test revealed signifi cantly reduced ATP in both OB (p=0.001) and OB+GDM (p<0.01) compared to NW. No diff erences were found between OB and OB+GDM (Fig.1). Conclusion: We hypothesized altered ATP production in placentas of OB/OB+GDM women. We found lower ATP content in cases vs NW placentas, suggesting possible inability of obese placentas to produce the required ATP and/or an excessive ATP turnover, indicating compromised placental function. At molecular level, ATP is produced by ATP synthase in the mitochondrial inner membrane. Interestingly, we previously showed dysfunctional features of placental mitochondria in OB/OB+GDM mothers. The current fi nding reinforces our hypothesis of altered mitochondrial function in these placentas. Further studies are ongoing to unravel molecular mechanisms involved in decreased placental ATP levels in OB/OB+GDM.