Diego Gomes Ferreira

PP181. The role of the JAK–STAT pathways and SOCS in preeclampsia

decreases insulin sensitivity and is associated with obesity. Recent data indicates that subclinical endotoxemia is associated with inflammation in obese women in late pregnancy. Objectives: The objective of this study was to quantify circulating endotoxin across pregnancy in lean and obese women, and assess the relationship between endotoxin and markers of inflammation and insulin sensitivity. Methods: Endotoxin was measured in sterile maternal EDTA plasma samples from 24 lean pregnant women (BMI = 22.4 ± 1.9 kg/m) and 45 obese pregnant women (BMI= 32.6 ± 2.1 kg/m), and 6 non-pregnant women. Samples were collected at 10.5 ± 3.1, 21.3 ± 4.6 and 35.2 ± 2.1 weeks gestation. Endotoxin was quantified using the PyroGene Recombinant Factor C endotoxin detection assay from LONZA, inter-assay variability <10%. IL-6, myloperoxidase, uric acid, triglycerides, insulin and glucose were also measured. Statistical analysis was by repeated measures ANOVA and students t-test as appropriate. Correlation analysis was performed using Pearson product moment correlation coefficient. Statistical significance was accepted at p < 0.05. Results: Endotoxin was significantly increased in both lean (10.4 ± 5.3 EU/ml) and obese (9.1 ± 5.3 EU/ml) pregnant women compared to non-pregnant women (4.3 ± 2.6 EU/ml, p < 0.05). Endotoxin increased significantly across pregnancy in both lean and obese pregnant women (p < 0.001), but was not different between these groups (table). Endotoxin was not associated with adiposity, IL-6, myloperoxidase, uric acid, triglycerides or insulin sensitivity as assessed by homeostasis model of insulin resistance (HOMA). Data are mean ± SD. Repeatedmeasures ANOVA p<0.001.