201-OR: Fasting and Postprandial Triglycerides in Early Pregnancy Correlate with Mean Glucose and Time-in-Range by CGM at 28 Weeks of Gestation

Recent studies of obesity in pregnancy have demonstrated a link between higher maternal fasting and postprandial triglycerides (FTG, PPTG) and neonatal subcutaneous and liver fat. Maternal TG can be hydrolyzed by placental lipases to free fatty acids (FFA) for fetal fat accretion, which may be further stimulated by fetal hyperinsulinemia from maternal glucose exposure. We hypothesized that higher FTG and PPTG in early pregnancy are predictive of abnormal glucose metabolism later in pregnancy at 28 weeks gestation using a point-of-care (POC) TG meter and continuous glucose monitor (CGM) metrics that have been associated with fetal overgrowth. At 15.4±0.9 weeks gestation (Mean±SD; early pregnancy), 31 healthy pregnant participants who were overweight or obese (32±5 years; pre-pregnancy BMI 30.6±3.0 kg/m²; 81% White, 19% Hispanic/Latino) were provided an FDA-approved POC TG meter to measure FTG and 2-hr PPTG after each meal for 4 days on an ad libitum diet. At 22, 28, and 34 weeks, 4 days of FTG and PPTG measures were repeated; a CGM was worn at 15 and 28 weeks. In early pregnancy across 119 fasting samples, the average median FTG was 126 mg/dL (68 - 191) and across 329 postprandial samples, the 2-hr PPTG was 153 mg/dL (92 - 247) at 15.4 weeks. At 28 weeks, the mean 24-hr glucose was 100±9 mg/dL and % time-in-range (%TIR 63-140 mg/dl) was 94±6% by CGM. Early FTG were positively correlated with mean 24-hr glucose at 28 weeks (r=0.41; p=0.02) and negatively correlated with %TIR (r=-0.44; p=0.01) by CGM. Moreover, early PPTG correlated with mean 24-hr glucose at 28 weeks (r=0.38; p=0.03). By associating ~450 TG measures with CGM metrics, these data suggest that TG concentrations during early pregnancy in obesity may identify women at risk for higher glycemic measures later in pregnancy. Because both TG and glucose contribute to excess infant adiposity, the timing, interaction, and contribution of both exposures to excess fetal fat deposition warrant further investigation.