AI Article Synopsis
- A study was conducted to investigate how human type 1 diabetic pregnancies affect the blood flow in the placenta and fetuses of rats, focusing on the differences between hyperglycemic (high blood sugar) and control groups.
- The research involved comparing 10 hyperglycemic rat mothers (with 107 fetuses) to 20 control mothers (with 219 fetuses) using Doppler ultrasound to measure blood flow and analyzing the placentas afterwards for various structural and inflammatory markers.
- Results showed that fetuses from hyperglycemic mothers had higher blood flow pulsatility indices, increased placental size, and changes in key gene expressions and inflammatory markers, indicating compromised fetal and placental health in diabetic conditions.
Article Abstract
Introduction: Human type 1 diabetic pregnancy is associated with placental structural and hemodynamic abnormalities. We hypothesized that in rat fetuses of hyperglycemic dams, placental and fetal blood flow velocity waveforms demonstrate compromised hemodynamics when compared to control fetuses, and these hemodynamic parameters correlate with placental structural abnormalities at near term gestation.
Methods: Streptozotocin-induced maternal hyperglycemia group comprised 10 dams with 107 fetuses and the control group 20 dams with 219 fetuses. Doppler-ultrasonographic examinations were performed at gestational days 13-14, 16-17, and 19-21. After the last examination, placentas were collected for morphologic, gene expression, and cytokine analysis.
Results: Umbilical artery (UA), descending aorta (DAO), and ductus venosus (DV) pulsatility indices (PI) were significantly higher at each study point in maternal hyperglycemia compared to controls. Placental size, glycogen storages, venous thrombosis formation, and fluid accumulation were increased in maternal hyperglycemia. Epidermal growth factor receptor (Edgfrb), platelet derived growth factor receptor beta polypeptide (Pdgfrb), and tumor necrosis factor receptor superfamily, member 12α (Tnfrsf12α) expressions were decreased. Interleukin (IL) -2 and -4 concentrations were decreased, and IL-1beta levels were increased in maternal hyperglycemia. UA PIs correlated positively with DV PIV, DAO PI, fluid accumulation, and glycogen storages. UA PIs correlated negatively with IL-4, Edgfrb, and Pdgfrb.
Discussion: In maternal hyperglycemia, placental and fetal hemodynamics were compromised during the last trimester of pregnancy compared to normoglycemic pregnancies. Placental structural, metabolic, and growth related gene expression, and inflammatory marker abnormalities were associated with hemodynamic compromise.
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| http://dx.doi.org/10.1016/j.placenta.2016.06.002 | DOI Listing |
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